Vesicle fusion mechanisms mediated by synaptosomal-associated protein 25 and its role in insulin secretion defects in type 2 diabetes mellitus
- VernacularTitle:突触相关蛋白25介导的囊泡融合机制及其在2型糖尿病胰岛素分泌障碍中的作用
- Author:
Jingbo ZHU
1
;
Kaiwen YU
;
Yating LU
;
Yan LU
Author Information
- Keywords: type 2 diabetes mellitus; insulin secretion; vesicle fusion defect; soluble N-ethyl-maleimide-sensitive factor attachment protein receptor; synaptosomal-associated protein 25; therapeu-tic target; genetic polymorphism
- From: Journal of Clinical Medicine in Practice 2025;29(13):137-144
- CountryChina
- Language:Chinese
- Abstract: The occurrence and development of type 2 diabetes mellitus(T2DM)are closely as-sociated with defects in insulin secretion.Synaptosomal-associated protein 25(SNAP25),as a core component of the soluble N-ethylmaleimide-sensitive factor attachment protein receptor(SNARE)complex,directly mediates the fusion of insulin secretion granules with the cell membrane and regu-lates the dynamic balance of insulin secretion stimulated by glucose.The expression defect of SNAP25 in patients with T2DM and model animals directly leads to vesicle fusion disorder,constituting the core pathological link of insulin secretion disorder and exacerbating the deterioration of β-cell func-tion.SNAP25 may serve as a key hub for multi-target synergistic intervention,and its genetic poly-morphism and the plasticity of its regulatory network offer novel strategies for precision therapy.This article innovatively integrated multidimensional regulatory mechanisms,including calcium channel ac-tivity,G-protein-coupled signaling and epigenetic modifications,to systematically analyze the spatio-temporal-specific regulatory network of SNAP25 in insulin secretion,providing a theoretical basis for T2DM therapeutic strategies targeting vesicle fusion.
