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Vagal nerve innervation divergence in liver/pancreas:A forgotten key to endocrine recovery after transplantation? 认领 引用
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作者 Ao-Yun Zhang Zi-Han Guo +6 位作者 Yuan Huang Yu-Rou Shi Xiao Song Shuai-Yan Wang Guan-Hu Yang Yun Liu Tian-Cheng Xu 《World Journal of Transplantation》 2026年第2期138-148,共11页
As the cross talk of the parasympathetic nervous system,the vagus nerve exerts organ-specific regulatory effects on hepatic and pancreatic endocrine homeostasis,yet its divergent innervation patterns and their implica... As the cross talk of the parasympathetic nervous system,the vagus nerve exerts organ-specific regulatory effects on hepatic and pancreatic endocrine homeostasis,yet its divergent innervation patterns and their implications for post-transplant functional recovery remain understudied.This review summarizes the anatomical and functional differences of the vagus nerve in the liver and pancreas,and discusses how surgical denervation and incomplete re-innervation affect endocrine recovery after liver and pancreatic transplantation.At the anatomical level,vagus nerve fibers in the liver are relatively sparse and travel along the portal tripa,mainly terminating in the perihilar blood vessels and biliary tract ecological loci,with limited direct parenchymal synapses.This structure is conducive to metabolic perception and indirect regulation of liver glucose flux,bile acid-dependent signaling,and inflammatory tension.In contrast,pancreatic vagus nerve input enters through periarterial/periductal channels and is relays through pancreatic ganglia,forming dense cholinergic efferent control over pancreatic isletα/β/δcells,supporting rapid and precise insulin-glucagon coordination and counterregulation responses.Clinically,recent preclinical trials and translational studies demonstrate that vagal nerve integrity-often compromised during transplant surgery-serves as a pivotal prognostic marker for endocrine recovery:Preserved vagal innervation is associated with accelerated glucose metabolism normal ization and reduced post-transplant complications(e.g.,insulin resistance,graft rejection).Notably,frontier strategies such as intraoperative vagal nerve-sparing techniques,targeted neuromodulation(e.g.,vagus nerve stimulation),and stem cell-derived neurotrophic factor delivery have shown promising potential in mitigating denervation-induced endocrine dysfunction.This review emphasizes that deciphering the organ-specific vagal innervation mechanisms holds great promise for optimizing precision transplant surgery and developing novel neuromodulatory therapies,which may revolutionize the prognosis of liver and pancreatic transplant recipients. 展开更多
关键词 Vagal nerve Liver/pancreas Transplantation Endocrine homeostasis Organ-specific innervation Neuromodulation
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Triggering receptor expressed on myeloid cells 2-driven pancreatic macrophage crosstalk:Key regulator of obesity pathophysiology and metabolic dysregulation 认领 引用
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作者 Ao-Yun Zhang Cong-Yi Xie +6 位作者 Xiao Song Zi-Han Guo Yu-Rou Shi Shuai-Yan Wang Guan-Hu Yang Yun Liu Tian-Cheng Xu 《World Journal of Biological Chemistry》 2026年第2期47-57,共11页
Obesity,a global epidemic,is closely linked to metabolic complications like insulin resistance and type 2 diabetes.Pancreatic dysfunction(impaired islet secretion and local inflammation)is central to this deterioratio... Obesity,a global epidemic,is closely linked to metabolic complications like insulin resistance and type 2 diabetes.Pancreatic dysfunction(impaired islet secretion and local inflammation)is central to this deterioration,yet the underlying mechanisms remain unclear.Pancreatic macrophages regulate tissue inflammation and metabolic homeostasis,but their context-specific polarization in obesity is undefined.This review discusses the role of triggering receptor expressed on myeloid cells 2(TREM2)in modulating pancreatic macrophage behavior in the context of obesity,based on findings from diet-induced obese mouse models and ex vivo pancreatic analyses.Emerging evidence indicates that TREM2 expression is markedly upregulated in pancreatic macrophages of obese subjects,where TREM2-driven macrophage activation promotes pro-inflammatory cytokine release and disrupts macrophage-islet β-cell crosstalk.Transcriptomic profiling reveals that TREM2 signaling reshapes macrophage transcriptional landscapes,enhancing proinflammatory phenotypes while impairing islet-supporting capacity.Notably,macrophage-specific TREM2 ablation has been shown to ameliorate pancreatic inflammation,restore islet insulin secretion,and alleviate systemic metabolic disorders in obese mice.Collectively,these findings identify TREM2 as a pivotal molecular switch governing pancreatic macrophage-mediated metabolic dysfunction in obesity,highlighting TREM2+pancreatic macrophages as a potential therapeutic target.These findings advance the understanding of immunemetabolic crosstalk in the pancreas,laying a foundation for developing novel immunometabolic interventions. 展开更多
关键词 Triggering receptor expressed on myeloid cells 2 Obesity Pancreatic macrophages Pancreatic inflammation Immunometabolism
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