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Biomarkers for synaptic dysfunction in Alzheimer’s disease 认领 引用 被引量：2
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作者 Ruiqing Ni 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第2期683-684,共2页
Alzheimer’s disease(AD)is the most common cause of dementia,characterized by progressive cognitive decline,and affects over 55 million people worldwide.AD is pathological featured by the aberrant accumulation of amyl... Alzheimer’s disease(AD)is the most common cause of dementia,characterized by progressive cognitive decline,and affects over 55 million people worldwide.AD is pathological featured by the aberrant accumulation of amyloid-βplaques,neurofibrillary tangles formed by hyperphosphorylated tau,synaptic loss,and dysfunction of neurotransmitter systems.Evidence from in vivo and autopsy studies has consistently shown that synaptic dysfunction and loss are strongly correlated with cognitive decline in AD,particularly in brain regions such as the hippocampus and cortex,which are critical for memory formation and processing.This perspective highlights recent histopathological findings related to synaptic dysfunction in AD,advancements in the development of imaging and fluid-based biomarkers for synaptic loss,and future studies. 展开更多
关键词 vivo autopsy studies synaptic dysfunction loss alzheimer s disease ad amyloid plaques cognitive declineand Alzheimers disease dysfunction neurotransmitter systemsevidence synaptic dysfunction
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Correlation between non-alcoholic fatty liver disease and erectile dysfunction:A systematic narrative review 认领 引用
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作者 Yan-Fei He Ning Bian +6 位作者 Huan-Zhi Wang Xiao-Dong Hu Jun-Qiang Liu Shuang-Feng Lu Ni Wu Qin-Tong He Hu-Ming Li 《World Journal of Hepatology》 2026年第4期190-199,共10页
BACKGROUND Non-alcoholic fatty liver disease(NAFLD)is the most common chronic liver disease worldwide,as well as a growing public health concern.Erectile dysfunction(ED)is one of the most common sexual dysfunctions in... BACKGROUND Non-alcoholic fatty liver disease(NAFLD)is the most common chronic liver disease worldwide,as well as a growing public health concern.Erectile dysfunction(ED)is one of the most common sexual dysfunctions in men.Currently,clinical research on the relationship between NAFLD and ED is limited.AIM To systematically review and narrative synthesize the existing evidence on the association between NAFLD and ED,and to elucidate potential underlying mechanisms.METHODS We conducted a comprehensive search of various electronic databases to identify original observational studies investigating the association between NAFLD and ED.However,due to significant heterogeneity among the included studies and the limited number of eligible investigations,we opted for a narrative synthesis instead of a meta-analysis.RESULTS A total of seven observational studies,involving 4442 participants(2043 of whom had NAFLD),were included in the analysis.The evidence consistently indicates a significant positive association between NAFLD and ED.Key influencing factors identified across the studies included age,components of metabolic syndrome,insulin resistance,serum testosterone levels,and psychological factors such as anxiety.CONCLUSION Existing evidence indicates a strong correlation between NAFLD and ED.The strength of this association is influenced by various factors,including age,insulin resistance,testosterone levels,and anxiety.NAFLD is an important risk factor for ED.Further high-quality studies are needed to confirm this relationship and explain its underlying mechanisms. 展开更多
关键词 Non-alcoholic fatty liver disease Erectile dysfunction Chronic liver diseases Sexual dysfunction Metabolic syndrome Insulin resistance Systematic review Narrative synthesis
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Do biomarkers matter?Cardiovascular risk stratification in Asian patients with metabolic dysfunction-associated steatotic liver disease in the era of fibrosis-centric assessment 认领 引用
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作者 Manjeet Kumar Goyal Juniali Hatwal +2 位作者 Rupak Desai Tanisha Sehgal Akash Batta 《World Journal of Gastroenterology》 SCIE CAS 2026年第28期10-18,共9页
Metabolic dysfunction-associated steatotic liver disease(MASLD)is increasingly recognized as a multisystem disorder with significant cardiovascular implications,particularly in Asian populations characterized by a hig... Metabolic dysfunction-associated steatotic liver disease(MASLD)is increasingly recognized as a multisystem disorder with significant cardiovascular implications,particularly in Asian populations characterized by a high prevalence of lean phenotypes and early metabolic dysregulation.Identifying reliable biomarkers for cardiovascular risk stratification in this group remains a clinical priority.This review critically appraises the current evidence on metabolic,inflammatory,cardiac,and fibrosis-related biomarkers in Asian patients with MASLD.Metabolic indices such as the uric acid-to-high-density lipoprotein ratio and triglycerideglucose index capture underlying insulin resistance and oxidative stress and show consistent associations with steatotic liver disease.However,direct validation for cardiovascular outcomes remains limited.Inflammatory markers,including highsensitivity C-reactive protein and homeostasis model assessment of insulin resistance,are mechanistically important but are confounded by their inclusion within MASLD diagnostic criteria,limiting their incremental predictive value.Cardiac biomarkers such as high-sensitivity troponins and natriuretic peptides demonstrate strong associations with adverse outcomes but lack sufficient validation in Asian MASLD cohorts for routine screening.In contrast,fibrosis-based indices,particularly the fibrosis-4 score,consistently associate with cardiovascular events,coronary artery calcification,and mortality across multiple Asian studies.These markers likely reflect cumulative metabolic and inflammatory injury linking hepatic and vascular pathology.An integrated,multivariable approach incorporating fibrosis markers alongside metabolic and cardiac indices may provide the most clinically meaningful framework for cardiovascular risk assessment in Asian patients with MASLD. 展开更多
关键词 Cardiovascular diseases Metabolic dysfunction-associated steatotic liver disease Obesity Uric acid Endothelial dysfunction High-density lipoprotein cholesterol Framingham risk score
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Surgical and anesthetic rewiring of the glymphatic system in postoperative cognitive dysfunction 认领 引用
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作者 Bandy Chen 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第9期4271-4272,共2页
Postoperative cognitive dysfunction(POCD)is a condition characterized by a variety of neurological deficits,including memory deficits,difficulty with attention and executive function,and behavioral changes or delirium... Postoperative cognitive dysfunction(POCD)is a condition characterized by a variety of neurological deficits,including memory deficits,difficulty with attention and executive function,and behavioral changes or deliriumlike symptoms.These changes can be transient or long-lasting;however the exact mechanisms involved in POCD pathogenesis remain unclear.Well-established pathways that can contribute to POCD are neuroinflammation,blood-brain barrier disruption,and neurovascular dysfunction. 展开更多
关键词 neurovascular dysfunction anesthetic memory deficitsdifficulty postoperative cognitive dysfunction deliriumlike symptomsthese postoperative cognitive dysfunction pocd behavioral changes glymphatic system
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Erectile dysfunction:Proposed definition and staging for early diagnosis 认领 引用
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作者 Arkiath Veettil Raveendran 《World Journal of Methodology》 2026年第1期61-69,共9页
Erectile dysfunction(ED)is considered a forerunner of cardiovascular disease.Early diagnosis of ED is important for identifying silent cardiovascular illness and reducing morbidity and mortality.ED has to be diagnosed... Erectile dysfunction(ED)is considered a forerunner of cardiovascular disease.Early diagnosis of ED is important for identifying silent cardiovascular illness and reducing morbidity and mortality.ED has to be diagnosed before it interferes with sexual function.Various aspects of ED,methods to assess ED,and different types of ED are briefly discussed in this article.The proposed definition and staging of ED help in early diagnosis and are expected to revolutionize the current concepts of diagnosis and management of ED. 展开更多
关键词 Erectile dysfunction Rigidity of penis Angle of erection Vaginal penetration pressure Post-ejaculatory refractory period Self-reported erection score Staging of erectile dysfunction Transient erectile dysfunction
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Modulation of mitochondrial dysfunction:Mechanisms and strategies for the use of natural products to treat stroke 认领 引用 被引量：2
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作者 Na Qin Rujuan Liu +3 位作者 Rong Deng Liuliu Shi Lei Wang Ting Zhu 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第6期2215-2226,共12页
Modulations of mitochondrial dysfunction,which involve a series of dynamic processes such as mitochondrial biogenesis,mitochondrial fusion and fission,mitochondrial transport,mitochondrial autophagy,mitochondrial apop... Modulations of mitochondrial dysfunction,which involve a series of dynamic processes such as mitochondrial biogenesis,mitochondrial fusion and fission,mitochondrial transport,mitochondrial autophagy,mitochondrial apoptosis,and oxidative stress,play an important role in the onset and progression of stroke.With a better understanding of the critical role of mitochondrial dysfunction modulations in post-stroke neurological injury,these modulations have emerged as a potential target for stroke prevention and treatment.Additionally,since effective treatments for stroke are extremely limited and natural products currently offer some outstanding advantages,we focused on the findings and mechanisms of action related to the use of natural products for targeting mitochondrial dysfunction in the treatment of stroke.Natural products achieve neuroprotective through multi-target regulation of mitochondrial dysfunction encompassing the following processes:(1)Mitochondrial biogenesis:Cordyceps and hydroxysafflor yellow A activate the peroxisome proliferator-activated receptor gamma coactivator 1-alphauclear respiratory factor pathway,promote mitochondrial DNA replication and respiratory chain protein synthesis,and thereby restore energy supply in the ischemic penumbra.(2)Mitochondrial dynamics balance:Ginsenoside Rb3 promotes Opa1-mediated neural stem cell migration and diffusion for recovery of damaged brain tissue.(3)Mitochondrial autophagy:Gypenoside XVII selectively eliminates damaged mitochondria via the phosphatase and tensin homolog-induced kinase 1/Parkin pathway and blocks reactive oxygen species and the NOD-like receptor protein 3 inflammasome cascade,thereby alleviating blood-brain barrier damage.(4)Anti-apoptotic mechanisms:Ginkgolide K inhibits Bax mitochondrial translocation and downregulates caspase-3/9 activity,reducing neuronal programmed death induced by ischemia-reperfusion.(5)Oxidative stress regulation:Scutellarin exerts antioxidant properties and improves neurological function by modulating the extracellular signal-regulated kinase 5-Kruppel-like factor 2-endothelial nitric oxide synthase signaling pathway.(6)Intercellular mitochondrial transport:Neuroprotective effects of Chrysophanol are associated with accelerated mitochondrial transfer from astrocytes to neurons.Existing studies have confirmed that natural products exhibit neuroprotective effects through multidimensional interventions targeting mitochondrial dysfunction in both ischemic and hemorrhagic stroke models.However,their clinical translation still faces challenges,such as the difficulty in standardization due to component complexity,insufficient cross-regional clinical data,and the lack of long-term safety evaluations.Future research should aim to integrate new technologies,such as single-cell sequencing and organoid models,to deeply explore the mitochondria-targeting mechanisms of natural products and validate their efficacy through multicenter clinical trials,providing theoretical support and translational pathways for the development of novel anti-stroke drugs. 展开更多
关键词 apoptosis autophagy hemorrhagic stroke ischemic stroke mitochondrial biogenesis mitochondrial dynamics mitochondrial dysfunction modulations mitochondrial transport natural products oxidative stress
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Near-infrared photobiomodulation therapy for age-related erectile dysfunction:molecular and physiological restoration in a mouse model 认领 引用 被引量：1
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作者 Zhong-Jie Zheng Yan Chen +5 位作者 Qian-Xi Chen Wen-Hao Tang Eric Chung Kai Hong Shu-Dong Zhang Hao-Cheng Lin 《Asian Journal of Andrology》 SCIE CAS CSCD 2026年第1期80-88,共9页
Age-related erectile dysfunction(ARED)represents a significant clinical challenge due to the interplay between chronic comorbidities and age-related physiological decline.This study investigated the therapeutic potent... Age-related erectile dysfunction(ARED)represents a significant clinical challenge due to the interplay between chronic comorbidities and age-related physiological decline.This study investigated the therapeutic potential of near-infrared photobiomodulation therapy(NIR-PBMT)in ARED mice,focusing on molecular and physiological mechanisms of complex erectile function restoration.Aged mice received NIR-PBMT(4 J cm−2)every 48 h for 2 weeks.Erectile function was evaluated using the maximum intracavernosal pressure/mean arterial pressure(ICPmax/MAP)ratio following cavernous nerve stimulation.Histological analysis and western blotting revealed significant improvements in penile tissue architecture,including increased smooth muscle content,reduced collagen deposition,and altered expression of senescence markers(p21 and phosphorylated H2A histone family member X[γ-H2A.X])and endothelial nitric oxide synthase(eNOS).In vitro studies using human corpus cavernous endothelial cells(HCCECs)demonstrated that NIR-PBMT reduced cellular senescence(assessed via SA-β-galactosidase staining),enhanced nitric oxide(NO)production,and improved mitochondrial network integrity.Angiogenesis assays further confirmed the pro-angiogenic effects of NIR-PBMT.Collectively,these findings highlight NIR-PBMT as a promising non-invasive therapy for ARED,acting through multiple pathways to reverse pathological remodeling and restore endothelial function.Future translational research is necessary to validate its clinical efficacy and optimize treatment protocols. 展开更多
关键词 age-related erectile dysfunction angiogenesis cellular senescence mitochondria near-infrared photobiomodulation therapy
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The ameliorative effects of ginger against heat-induced oxidative stress and mitochondrial dysfunction in Caenorhabditis elegans 认领 引用 被引量：1
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作者 Tingting Xu Mingfang Tao +6 位作者 Rong Li Shuxin Tang Yuting Huang Ting Wu Senem Kamiloglu Siyi Pan Xiaoyun Xu 《Food Science and Human Wellness》 SCIE CAS CSCD 2026年第4期1823-1838,共16页
Ginger,rich in gingerols and shogaols,exhibits multiple biological properties.However,the mechanisms underlying its thermotolerance remain unclear.The study employed network pharmacology and experimental validation in... Ginger,rich in gingerols and shogaols,exhibits multiple biological properties.However,the mechanisms underlying its thermotolerance remain unclear.The study employed network pharmacology and experimental validation in Caenorhabditis elegans to investigate how gingerol-related compounds within ginger extract(GE)mitigated damage caused by heat stress(HS).A total of 18 types of gingerol analogues were identified in GE,among which 6-,8-,and 10-gingerol,as well as 6-,8-,and 10-shogaol were quantified.Collectively,these 6 compounds accounted for 54.4%of the total composition.Supplementation with 15μg/m L GE significantly extended heatstress lifespan by 20.30%,while the combination of the 6 major gingerols and shogaols at the same concentration prolonged lifespan by 18.93%.Additionally,pretreatment with GE and the combination alleviated HS-induced oxidative damage by eliminating reactive oxygen species(ROS)and upregulating antioxidant enzymes.Network pharmacology analysis suggested that the MAPK pathway may play a crucial role in thermotolerance.Experimental findings confirmed that ginger attenuated oxidative damage through the activation of SKN-1/Nrf2 and DAF-16/FOXO via the MAPK pathway.Moreover,GE stabilized mitochondrial membrane potential and restored ATP levels,thus preserving mitochondrial function during heat exposure.Further investigations using molecular docking and molecular dynamics simulations revealed that shogaols,with more stable binding affinities for Keap1 protein,exhibited more potent effects than gingerols in prolonging lifespan and reducing ROS levels under HS conditions.In short,gingerol analogues from ginger conferred thermal resistance to nematodes by mitigating oxidative damage and mitochondrial dysfunction. 展开更多
关键词 Ginger Gingerols Shogaols Thermal tolerance Oxidative stress Mitochondrial dysfunction
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Neurogenic organ dysfunction syndrome after acute brain injury 认领 引用 被引量：1
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作者 Heng Zhang Wen-Jin Chen +14 位作者 Yan-Gong Chao Nan Su Chiara Robba Marek Czosnyka Peter Smielewski Zofia Czosnyka Wei He Xiao Hu De-Zhong Yao Cheng-Gong Hu Min Zhou Yun-Jie Wang Xiao-Chun Ma Xiu-Yun Liu Dong Ming 《Military Medical Research》 SCIE CAS CSCD 2026年第4期542-558,共17页
Systemic complications are common after acute brain injury(ABI)and may trigger coagulation cascades,systemic inflammation,as well as dysfunction of the cardiovascular,respiratory,and gastrointestinal systems,etc.The p... Systemic complications are common after acute brain injury(ABI)and may trigger coagulation cascades,systemic inflammation,as well as dysfunction of the cardiovascular,respiratory,and gastrointestinal systems,etc.The pathogenesis of these systemic manifestations is multifactorial but not yet fully elucidated.This paper introduces the novel term neurogenic organ dysfunction syndrome(NODS)to characterize systemic instability arising from internal and external perturbations of the neuronal center following ABI.Elucidating the central neurogenic mechanisms of NODS is critical for early detection and prevention of complications,thereby reducing mortality and improving patient outcomes following ABI.In this paper,we explore the potential central neurogenic mechanisms of NODS from the perspective of complex brain network theory,focusing on the structural network of the central autonomic system(CAS)that maintains systemic stability,and the functional network governed by the central stress system(CSS).The CAS can be divided into the cortical autonomic network,which involves higher cortical regions,and the subcortical autonomic network,which is relatively conserved,with its main connections located in deep brain structures.The CSS is a large-scale complex network characterized by hierarchy,hubs,and modularity,which together enable the competitive optimization of functional segregation and integration.Under physiological conditions,modules(mediating functional segregation)and hubs(functional integration)within the CSS dynamically trade-off with each other to maintain the overall homeostasis.However,this balance is disrupted following pathological insults or injury,resulting in weakened functional integrity of the CSS following ABI,impaired module activity,and disturbed hub integration.This paper also demonstrates the distinct pathological manifestations arising from disturbances at different levels of the homeostatic system.Finally,this study proposes potential clinical interventions,including analgesia and sedation,neuromodulation,and receptor regulation,for early interventions and potential treatment of NODS,aiming to improve patient outcomes. 展开更多
关键词 Neurogenic organ dysfunction syndrome Acute brain injury Hierarchical modular structure Hierarchical hub Small-world network Systemic homeostasis
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Shexiang Tongxin dropping pill improves homocysteine-induced coronary microvascular dysfunction via regulating PI3K/Akt/eNOS pathway 认领 引用
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作者 Shuai Li Zuxian Zhang +5 位作者 Ming Gong Xiaojun Li Xuan Jia Yijun Chen Xianwen Tang Wei Wang 《Journal of Traditional Chinese Medical Sciences》 CAS CSCD 2026年第1期77-89,共13页
Objective:To establish a mouse model of homocysteine(Hcy)-induced coronary microvascular dysfunction(CMD),and to evaluate the therapeutic efficacy of Shexiang Tongxin dropping pill(STDP)and elucidate its underlying me... Objective:To establish a mouse model of homocysteine(Hcy)-induced coronary microvascular dysfunction(CMD),and to evaluate the therapeutic efficacy of Shexiang Tongxin dropping pill(STDP)and elucidate its underlying mechanisms.Methods:The chemical composition and quality of STDP were characterized using ultra-high performance liquid chromatography,and its absorbed components were identified using ultra-high performance liquid chromatography with quadrupole time-of-flight mass spectrometry.CMD was induced in C57BL/6J mice by feeding a 3%methionine diet for four weeks.STDP efficacy was evaluated using laser speckle perfusion imaging,tomato lectin staining,and quantification of plasma nitric oxide(NO),reactive oxygen species(ROS),and endothelial adhesion molecules(intercellular cell adhesion molecule-1[ICAM-1],vascular cell adhesion molecule-1[VCAM-1]).Network pharmacology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses were performed to identify potential targets and regulatory pathways.An in vitro Hcy-induced endothelial injury model was used to validate the effects of STDP on cell viability,NO production,and activation of phosphatidylinositol 3-kinase/protein kinase B/endothelial nitric oxide synthase(PI3K/Akt/eNOS)pathway.Results:STDP was stable,with 180 constituents identified in the preparation and 30 absorbed components in plasma.STDP treatment restored perfusion,increased plasma NO,decreased ROS,and downregulated ICAM-1 and VCAM-1.Network analysis identified 152 putative targets,highlighting the PI3K/Akt pathway as the central,with PIK3CA,AKT1,and NOS3 as key nodes.In vitro,STDP enhanced cell viability,NO production,and PI3K/Akt/eNOS phosphorylation,these effects were abolished by pharmacological inhibition of PI3K and eNOS.Conclusion:A 3%methionine diet for four weeks effectively induces CMD in C57BL/6J mice.STDP,rich in bioactive components,alleviates Hcy-induced CMD by activating the PI3K/Akt/eNOS pathway,thereby improving endothelial function and microvascular perfusion.These findings support STDP as a promising therapeutic candidate for CMD management. 展开更多
关键词 Shexiang Tongxin dropping pill Homocysteine Coronary microvascular dysfunction Endothelial dysfunction PI3K/Akt/eNOS pathway
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Palmitic acid-induced autolysosomal dysfunction and lipotoxicity in neuroinflammation and neurodegeneration 认领 引用
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作者 Eka Norfaishanty Saipuljumri Jialiu Zeng Chih Hung Lo 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第7期2806-2811,共6页
Neurodegenerative disorde rs such as Alzheimer's and Parkinson s diseases are increasingly associated with metabolic dysfunction,including obesity,type 2 diabetes,and metabolic dysfunction-associated steatotic liv... Neurodegenerative disorde rs such as Alzheimer's and Parkinson s diseases are increasingly associated with metabolic dysfunction,including obesity,type 2 diabetes,and metabolic dysfunction-associated steatotic liver disease.Central to this connection is the dysregulation of lipid metabolism,which extends beyond peripheral tissues to the brain,defective autolysosomal function,oxidative stress,inflammation,and insulin resistance.Lipids,which constitute over half of dry weight of the brain,play critical roles in ene rgy provisio n,structural integrity,and synaptic function.Dys regulation of lipid metabolism contributes to neuroinflammation,impaired neuronal function,and disrupted blood-brain barrier integrity.Palmitic acid,a saturated fatty acid abundant in high-fat diets,serves as a key model for studying lipid-induced toxicity(lipotoxicity)in the brain.Palmitic acid disrupts autophagy and lysosomal function,mitochondrial function,trigge ring oxidative stress,contributing to neuroinflammation and neurodegeneration.These effects are particularly pronounced in neurons,which are highly susceptible to lipid-induced toxicity due to their high metabolic demands.Glial cells,including astrocytes,microglia,and oligodendrocytes,also exhibit distinct vulnerabilities and adaptive responses to lipid metabolism dysregulation,further contributing to neuroinflammation and demyelination.Therapeutic strategies,such as supplementation with polyunsaturated fatty acids,AMP-activated protein kinase activation,and lysosome-ta rgeted interventions,show promise in mitigating palmitic acid-induced lipotoxicity and restoring cellular homeostasis.This review comprehensively examines palmitic acid-induced lipotoxicity and its impact on autolysosomal dysfunction across various central nervous system cell types,including neurons,astrocytes,microglia,and oligodendrocytes.Additionally,it highlights therapeutic approaches to restore autolysosomal function under lipotoxic conditions.Advances in multi-omics technologies and a deeper unde rstanding of intercellular crosstalk offer new avenues for develo ping targeted the rapies to resto re autolysosomal function,and attenuate neuroinflammation and neurodegeneration. 展开更多
关键词 autolysosomal dysfunction lipotoxicity metabolic dysfunction neuroinflammation palmitic acid
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Mitochondrial Dysfunction as a Pathophysiological Bridge between Metabolic Dysfunction-Associated Fatty Liver Disease and Chronic Kidney Disease 认领 引用
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作者 Congwei You Anwen Yin +3 位作者 Jia Xia Le Zhang Xiaolei Wang Yutong Hou 《BIOCELL》 SCIE 2026年第3期24-46,共23页
Metabolic dysfunction-associated fatty liver disease(MAFLD)and chronic kidney disease(CKD)have shown a marked global increase in prevalence,placing a substantial burden on public health and healthcare systems worldwid... Metabolic dysfunction-associated fatty liver disease(MAFLD)and chronic kidney disease(CKD)have shown a marked global increase in prevalence,placing a substantial burden on public health and healthcare systems worldwide.Epidemiological data demonstrate a significant overlap between these two conditions,with further evidence from research identifying common pathophysiological features,such as lipid metabolism dysregulation,disrupted energy balance,and chronic systemic inflammation.Mitochondria are central to the pathophysiology of both diseases.In addition to their role in energy production,mitochondria are involved in numerous critical cellular processes,including biosynthesis,lipid metabolism,oxidative phosphorylation,signal transduction,and apoptosis regulation.Mitochondrial dysfunction,characterized by increased reactive oxygen species,impaired adenosine triphosphate synthesis,disrupted mitophagy,and changes in mitochondrial morphology,is implicated in the progression of both MAFLDandCKD.Given the pivotal role of mitochondria in maintaining cellularmetabolism homeostasis,dysfunction of this organelle is increasingly recognized as a key mechanistic link that connects the pathophysiological processes underlying both MAFLD and CKD.This review underscores mitochondrial dysfunction as a pathogenic nexus between MAFLD and CKD and examines the mechanisms that drive their pathogenesis. 展开更多
关键词 Mitochondrial dysfunction oxidative stress lipid metabolism metabolic dysfunction-associated fatty liver disease(MAFLD) chronic kidney disease(CKD) liver-kidney crosstalk
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Metabolic dysfunction-associated steatotic liver disease and heart failure with preserved ejection fraction:A state-of-the-art review 认领 引用
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作者 Ajit Singh Brar Tejasvini Khanna +6 位作者 Aalam Sohal Juniali Hatwal Vishal Sharma Carol Singh Akash Batta Praveen Chandra Bishav Mohan 《World Journal of Cardiology》 2026年第1期29-55,共27页
Metabolic dysfunction-associated steatotic liver disease(MASLD)has rapidly become the leading cause of chronic liver disease and cirrhosis worldwide,driven by the global surge in metabolic disorders such as obesity,di... Metabolic dysfunction-associated steatotic liver disease(MASLD)has rapidly become the leading cause of chronic liver disease and cirrhosis worldwide,driven by the global surge in metabolic disorders such as obesity,diabetes,hypertension,and dyslipidemia.In parallel,heart failure with preserved ejection fraction(HFpEF)has surpassed heart failure with reduced ejection fraction(HFrEF)as the predominant form of heart failure,particularly in individuals with metabolic comorbidities.Mounting evidence points to a significant overlap in the pathophysiological underpinnings of MASLD and HFpEF,with metabolic dysfunction serving as a common foundation.This review synthesizes current knowledge on the mechanistic links between MASLD and HFpEF,examining metabolic,inflammatory,and fibrotic pathways.We also explore the clinical implications of this association,including diagnostic considerations and therapeutic targets.Shared risk factors and inflammatory pathways have highlighted a strong bidirectional association between MASLD and cardiovascular diseases,particularly HFpEF.Significantly,the degree of hepatic fibrosis in MASLD correlates with HFpEF prognosis and severity,emphasizing the systemic nature of these conditions.Emerging pharmacological and lifestyle-based interventions aimed at managing both conditions underscore the importance of integrated,multidisciplinary care in improving long-term outcomes. 展开更多
关键词 Metabolic dysfunction-associated steatotic liver disease Heart failure with preserved ejection fraction Diabetes mellitus Obesity Hypertension Dyslipidemia Obstructive sleep apnea Inflammation Metabolic dysfunction
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High-fat diet,gut dysbiosis,and oxidative stress:A synergistic triangle in metabolic dysfunction-associated steatotic liver disease pathogenesis 认领 引用
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作者 Zi-Rui Zhang Ling She +1 位作者 Yi-Rong Cao Yuan-Wen Chen 《World Journal of Hepatology》 2026年第4期37-53,共17页
Metabolic dysfunction-associated steatotic liver disease(MASLD)is a prominent metabolic disease characterized by hepatic steatosis,inflammation,and progressive liver damage,in which oxidative stress plays a crucial pa... Metabolic dysfunction-associated steatotic liver disease(MASLD)is a prominent metabolic disease characterized by hepatic steatosis,inflammation,and progressive liver damage,in which oxidative stress plays a crucial pathogenic role.Increasing attention has been drawn to the contributions of a high fat diet(HFD)and gut dysbiosis in the onset and progression of MASLD.These factors compromise intestinal barrier integrity,promote endotoxemia,induce lipid peroxidation,and activate pro-inflammatory signaling pathways,contributing to oxidative stress.Excessive production of reactive oxygen species disrupts hepatic redox homeostasis,impairs mitochondrial function,and amplifies inflammatory responses,thereby accelerating hepatic fibrosis and disease progression.This review highlights the triangular and synergistic relationship among HFD,gut dysbiosis,and oxidative stress in MASLD pathogenesis.It provides a comprehensive overview of antioxidant interventions,including lifestyle modifications,dietary antioxidants,natural bioactive compounds,and pharmacological agents,aiming at providing promising MASLD management in future clinical applications. 展开更多
关键词 Metabolic dysfunction-associated steatotic liver disease High-fat diet Gut dysbiosis Oxidative stress Intestinal barrier dysfunction
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Fucosylated IgG Contributes to Adipose Tissue Dysfunction During Aging 认领 引用
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作者 Jingyu Wang Wei Su +3 位作者 Haotian Wang Licui Liu Jinlong Li Youxin Wang 《Engineering》 SCIE EI CSCD 2026年第2期149-158,共10页
Immunoglobulin G(IgG)is recognized as a key regulator of metabolic dysfunction and fibrosis in adipose tissue,and its functional properties are tightly regulated by its glycosylation profile.However,the role of Ig G g... Immunoglobulin G(IgG)is recognized as a key regulator of metabolic dysfunction and fibrosis in adipose tissue,and its functional properties are tightly regulated by its glycosylation profile.However,the role of Ig G glycosylation in adipose aging remains unclear.Here,we performed transcriptomic and glycoproteomic analyses of epididymal white adipose tissue(eWAT)from young and aged mice.RNA sequencing(RNA-seq)analysis revealed a significant downregulation of adipogenic genes in aged eWAT,accompanied by elevated expression levels of inflammatory and fibrotic markers,which were further validated by quantitative polymerase chain reaction(qPCR).N-and O-glycoproteomic analyses revealed widespread changes in glycosylation.Differentially glycosylated proteins are primarily localized to the extracellular space and participate in innate immune responses,transport and signal transduction,extracellular matrix(ECM)–receptor interaction pathways,and so on.Notably,IgG glycosylation levels were significantly increased in aged mice.Specifically,the N-fucosylation of IgG1,IgG2a,and IgG3 was elevated by 3.1-,10.4-,and 3.2-fold,respectively,while only IgG2a showed increased O-fucosylation.These findings suggest that N-fucosylation is a common age-related modification across IgG subtypes.Using in vivo models,we further demonstrated that B-cell depletion-induced IgG reduction increased adipogenic and inflammatory gene expression,while the expression of fibrotic markers was suppressed.These effects were reversed upon repletion with either fucosylated or nonfucosylated IgG.Importantly,compared with nonfucosylated IgG,fucosylated IgG exacerbated inflammation and fibrosis but inhibited adipogenesis more strongly.Taken together,our results identify fucosylated IgG as a key mediator of adipose dysfunction during aging and suggest that modulating IgG fucosylation may offer therapeutic potential for age-related metabolic disorders. 展开更多
关键词 Immunoglobulin G Fucosylation Adipose tissue aging Glycosylation Metabolic dysfunction Fibrosis
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Systematic review of mitochondrial dysfunction and oxidative stress in aging:A focus on neuromuscular junctions 认领 引用
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作者 Senlin Chai Ning Zhang +8 位作者 Can Cui Zhengyuan Bao Qianjin Wang Wujian Lin Ronald Man Yeung Wong Sheung Wai Law Rebecca Schönmehl Christoph Brochhausen Wing Hoi Cheung 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第5期1947-1960,共14页
Mitochondrial dysfunction and oxidative stress are widely regarded as primary drivers of aging and are associated with several neurodegenerative diseases.The degeneration of motor neurons during aging is a critical pa... Mitochondrial dysfunction and oxidative stress are widely regarded as primary drivers of aging and are associated with several neurodegenerative diseases.The degeneration of motor neurons during aging is a critical pathological factor contributing to the progression of sarcopenia.However,the morphological and functional changes in mitochondria and their interplay in the degeneration of the neuromuscular junction during aging remain poorly understood.A defined systematic search of the Pub Med,Web of Science and Embase databases(last accessed on October 30,2024)was conducted with search terms including'mitochondria','aging'and'NMJ'.Clinical and preclinical studies of mitochondrial dysfunction and neuromuscular junction degeneration during aging.Twentyseven studies were included in this systematic review.This systematic review provides a summary of morphological,functional and biological changes in neuromuscular junction,mitochondrial morphology,biosynthesis,respiratory chain function,and mitophagy during aging.We focus on the interactions and mechanisms underlying the relationship between mitochondria and neuromuscular junctions during aging.Aging is characterized by significant reductions in mitochondrial fusion/fission cycles,biosynthesis,and mitochondrial quality control,which may lead to neuromuscular junction dysfunction,denervation and poor physical performance.Motor nerve terminals that exhibit redox sensitivity are among the first to exhibit abnormalities,ultimately leading to an early decline in muscle strength through impaired neuromuscular junction transmission function.Parg coactivator 1 alpha is a crucial molecule that regulates mitochondrial biogenesis and modulates various pathways,including the mitochondrial respiratory chain,energy deficiency,oxidative stress,and inflammation.Mitochondrial dysfunction is correlated with neuromuscular junction denervation and acetylcholine receptor fragmentation,resulting in muscle atrophy and a decrease in strength during aging.Physical therapy,pharmacotherapy,and gene therapy can alleviate the structural degeneration and functional deterioration of neuromuscular junction by restoring mitochondrial function.Therefore,mitochondria are considered potential targets for preserving neuromuscular junction morphology and function during aging to treat sarcopenia. 展开更多
关键词 aging mitochondrial dysfunction neuromuscular junction oxidative stress sarcopenia systematic review
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Loss of PTH 1 receptor signaling in periodontal cells drives cementum dysfunction and molar ankylosis in mice 认领 引用
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作者 Hakan Turkkahraman Carson Joseph Walton +4 位作者 Tianli Zhu Nisreen Akel Silvia Marino Xue Yuan Teresita M.Bellido 《Bone Research》 SCIE CAS CSCD 2026年第3期892-901,共10页
Parathyroid hormone 1 receptor(PTH1R)signaling is critical for mineral ion homeostasis and skeletal development.Although its role in tooth root formation and eruption is established,its specific functions in adult per... Parathyroid hormone 1 receptor(PTH1R)signaling is critical for mineral ion homeostasis and skeletal development.Although its role in tooth root formation and eruption is established,its specific functions in adult periodontal tissues and craniofacial integrity remain incompletely defined.Here,we investigated the craniofacial and dentoalveolar phenotypes of mice with conditional deletion of PTH1R in DMP1-Cre-expressing cells.DMP1-Cre;PTH1Rfl/flmutant mice exhibited craniofacial alterations,including reduced maxillary length and defects in the alveolar bone surrounding the molars,as revealed by micro-computed tomography and histological analysis.The mutant mice also displayed severe periodontal ligament(PDL)loss and extensive molar ankylosis,characterized by the direct fusion of alveolar bone to tooth roots,predominantly in regions of acellular cementum.In contrast,incisor development remained unaffected.PTH1R deficiency also resulted in pathological cementum overgrowth,disrupted PDL fiber organization,and decreased expression of key PDL matrix proteins,as evidenced by immunohistochemical and molecular analyses.Mechanistically,the loss of PTH1R enhanced Smad3 phosphorylation and upregulated Osterix,thereby promoting aberrant cementoblast differentiation and mineralization.Concurrently,Dkk1 expression was increased,leading to suppressed Wnt signaling.This evidence establishes PTH1R signaling in cementocytes as a central safeguard of cementum homeostasis and PDL integrity and demonstrates that its disruption induces pathological root-bone fusion and craniofacial abnormalities.These findings advance our understanding of the molecular mechanisms underlying adult periodontal tissue maintenance and open new opportunities for developing therapeutic strategies against ankylosis and related disorders by targeting PTH1R signaling. 展开更多
关键词 mineral ion homeostasis craniofacial cementum dysfunction tooth root formation eruption craniofacial alterationsincluding skeletal developmentalthough PTH R craniofacial integrity
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Xijiaqi Formula attenuates cognitive dysfunction by inhibiting neuroinflammation and promoting neuroplasticity in rats with chronic heart failure 认领 引用
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作者 Jie Chen Xuefen Wu +8 位作者 Qian Zhang Hongcai Shang Wanting Li Linnan Zhou Xinyu Chu Guiyang Xia Huan Xia Xiaohong Wei Sheng Lin 《Chinese Journal of Natural Medicines》 SCIE CAS CSCD 2026年第1期73-88,共16页
Chronic heart failure(CHF)impairs cognitive function.Xijiaqi Formula(XJQ),a traditional Chinese medicine(TCM)used clinically to treat CHF,demonstrates potential for improving cognition in CHF patients.However,its prec... Chronic heart failure(CHF)impairs cognitive function.Xijiaqi Formula(XJQ),a traditional Chinese medicine(TCM)used clinically to treat CHF,demonstrates potential for improving cognition in CHF patients.However,its precise mechanism in treating post-CHF cognitive dysfunction remains unclear.This study systematically investigates XJQ’s effects on post-CHF cognitive dysfunction and the underlying mechanisms.The components of XJQ were identified through liquid chromatography-mass spectrometry.CHF was induced in rats via ligation of the left anterior descending coronary artery,followed by six weeks of XJQ treatment.Cardiac function was evaluated through echocardiography and hemodynamic parameters,while cognitive function was assessed using Morris water maze(MWM)and open field tests(OFT).XJQ treatment enhanced both cardiac and cognitive functions in CHF rats.Network pharmacology identified 12 core active components of XJQ and indicated its effect on cognitive dysfunction involved regulating synapses,inflammation,and phosphodiesterase 4(PDE4)-dependent cyclic adenosine monophosphate(cAMP)signaling.XJQ inhibited microglial and astrocyte activation,decreased proinflammatory cytokines,and mitigated neuronal damage.Notably,XJQ promoted synaptic repair and dendritic growth by downregulating PDE4 and upregulating cAMP,protein kinase A(PKA),cAMP-response element binding protein(CREB),brain-derived neurotrophic factor(BDNF),PSD95,and synapsin I levels.Molecular docking and Bio-layer interferometry assays confirmed direct binding of quercetin,kaempferol,isorhamnetin,and darutoside to PDE4.In conclusion,XJQ alleviates neuroinflammation and enhances synaptic plasticity to improve cognitive dysfunction in CHF rats via the PDE4/cAMP/PKA/CREB signaling pathway.These findings provide valuable insight into the heart-brain axis. 展开更多
关键词 Xijiaqi Formula Cognitive dysfunction Chronic heart failure Synaptic plasticity Neuroinflammation PDE4
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Endothelial cell injury:a crucial link in microcirculatory dysfunction associated with sepsis 认领 引用
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作者 Yuhui Pan Yanyan Ma +3 位作者 Ke Wan Yizhou Xu Guoxing Wang Miaorong Xie 《World Journal of Emergency Medicine》 SCIE CAS CSCD 2026年第1期28-35,共8页
BACKGROUND:Sepsis is a prevalent and severe condition,with microcirculation disruptions playing a crucial role in its progression.Endothelial cell(EC)injury is the primary factor behind microcirculatory issues.This re... BACKGROUND:Sepsis is a prevalent and severe condition,with microcirculation disruptions playing a crucial role in its progression.Endothelial cell(EC)injury is the primary factor behind microcirculatory issues.This review is to outline the pathomechanism,organ heterogeneity,biomarkers,and therapeutic implications of endothelial dysfunction in sepsis,off ering references and insights for the clinical management of sepsis.METHODS:A systematic search of Web of Science and PubMed from inception to June 10,2025,limited to English publications,was conducted.Two reviewers independently identifi ed studies on EC injury in patients with septic microcirculatory dysfunction.Duplicate articles based on multiple search criteria were excluded.RESULTS:Fifty-nine articles,including cell,animal,and clinical studies,were included.These studies reported the effects of EC injury on the microcirculation in sepsis,including changes in vascular permeability,coagulation dysfunction,vasomotor regulation,and infl ammatory responses.These pathways interact and ultimately lead to septic microcirculation disorders.CONCLUSION:Sepsis-induced endothelial dysfunction involves various interconnected mechanisms,which collectively compromise ECs and impede microcirculatory perfusion.Future research should enhance current understanding of endothelial injury mechanisms,develop synergistic multi-target strategies to disrupt this cycle,and facilitate the clinical application of endothelial markers for early intervention and dynamic assessment. 展开更多
关键词 Sepsis Endothelial cells Vascular permeability Coagulation dysfunction Vasomotor regulation Infl ammatory responses Microcirculatory
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Nephropathy 1 Formula alleviates kidney injury by ameliorating mitochondrial dysfunction and pyroptosis in diabetic nephropathy through the TMAO-mROS-NLRP3 axis 认领 引用
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作者 Tingting Wei Yujiu Gao +9 位作者 Liting Zhu Congcong Zeng Rui Cai Fu Rao Yue Zhao Xiaochun Zhang Jiashun Yang Yinrui Sheng Zhengzhong Yuan Jinguo Cheng 《Chinese Journal of Natural Medicines》 SCIE CAS CSCD 2026年第4期454-469,共16页
Nephropathy 1 Formula(N1F),a traditional Chinese medicine(TCM),has demonstrated promising clinical efficacy in diabetic nephropathy(DN). However,its underlying protective mechanisms remain insufficiently defined. In t... Nephropathy 1 Formula(N1F),a traditional Chinese medicine(TCM),has demonstrated promising clinical efficacy in diabetic nephropathy(DN). However,its underlying protective mechanisms remain insufficiently defined. In this study,a type 2 diabetes mellitus(T2 DM)mouse model was established using a high-fat diet(HFD) and streptozotocin(STZ). Additionally,DN was simulated in vitro via exposure of mouse glomerular mesangial cells(MES-13) to high glucose(HG) and trimethylamine-N-oxide(TMAO). To elucidate the mechanistic basis of N1F's renoprotective effects,an integrative approach combining metabolomics,transcriptomics,and 16S ribosomal ribonucleic acid(rRNA) gene sequencing was employed. N1F treatment reduced the urinary albumin-to-creatinine ratio(UACR),preserved renal function,and attenuated histopathological damage and renal fibrosis in diabetic mice. Mechanistically,N1F modulated systemic TMAO levels and energy metabolism,altered gut microbiota composition,and suppressed microbial production of TMAO-related metabolites. Under hyperglycemic conditions,TMAO induced excessive mitochondrial reactive oxygen species(mROS),impaired mitochondrial dynamics,and disrupted cellular energy metabolism. In contrast,N1F normalized mROS levels,restored mitochondrial structure and function,enhanced oxidative phosphorylation(OXPHOS),increased ATP production,and reduced glycolytic dependency.Furthermore,N1F downregulated the expression of key pyroptosis-related proteins—including NOD-like receptor family pyrin domain-containing 3(NLRP3),N-terminal gasdermin D(GSDMD),cleaved-Casp1,interleukin-1β(IL-1β),and IL-18—in both in vivo and in vitro models,indicating suppression of pyroptosis via inhibition of the TMAO-mROS-NLRP3 signaling axis. Collectively,these findings demonstrate that N1F exerts protective effects against DN by targeting mitochondrial dysfunction and pyroptotic injury,supporting its potential as a therapeutic strategy for DN. 展开更多
关键词 Diabetic nephropathy Trimethylamine-N-oxide(TMAO) Mitochondrial dysfunction Pyroptosis
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