文献类型：期刊文献

中文题名：慢性炎症与纤维化相互作用在糖尿病肾病中作用的研究进展

英文题名：Research Progress on the Role of the Interaction Between Chronic Inflammation and Fibrosis in Diabetic Nephropathy

作者：徐进[1];李建省[1];刘臻华[2];张新丽[1]

第一作者：徐进

机构：[1]甘肃省中医院肾病科,兰州730000;[2]甘肃中医药大学,兰州730000

第一机构：甘肃省中医院肾病科,兰州730000

年份：2025

卷号：16

期号：4

起止页码：980

中文期刊名：协和医学杂志

外文期刊名：Medical Journal of Peking Union Medical College Hospital

收录：;北大核心:【北大核心2023】；

基金：国家自然科学基金(82160865);甘肃省中医药管理局?重点课题(GZKZ?2022?3)。

语种：中文

中文关键词：糖尿病肾病;炎症反应;肾纤维化;上皮-间质转化;细胞外基质;信号通路

外文关键词：diabetic nephropathy;inflammatory response;renal fibrosis;epithelial-mesenchymal transition;extracellular matrix;signal pathway

摘要：糖尿病肾病(diabetic nephropathy,DN)是糖尿病患者发展为终末期肾病(end-stage renal disease,ESRD)的主要原因,其核心病理特征包括慢性炎症和纤维化。慢性炎症通过激活免疫细胞、分泌促炎细胞因子以及启动多条信号通路,促进肾脏细胞损伤、上皮-间质转化和细胞外基质成分积累。细胞外基质过度沉积不仅破坏肾脏结构,还可导致肾小管间质扩展,进一步加剧肾脏功能衰退。近年来研究表明,慢性炎症与纤维化在DN进展中相辅相成,二者交互作用共同推动疾病恶化。炎症反应不仅是纤维化发生的早期驱动因素,还可通过多种反馈机制加剧纤维化进程,形成炎症-纤维化恶性循环。但慢性炎症与纤维化之间的具体分子机制尚未完全阐明,故深入探索慢性炎症与纤维化的相互作用机制对于防治DN至关重要。本文通过阐述慢性炎症、纤维化在DN中的作用机制,旨在深入理解DN的发生机制,为临床开发新的治疗方案提供参考与依据。
Diabetic nephropathy(DN),a primary cause of end-stage renal disease(ESRD)in diabetic patients,is pathologically characterized by chronic inflammation and renal fibrosis.Chronic inflammation promotes renal cellular damage,epithelial-mesenchymal transition,and extracellular matrix(ECM)accumulation through mechanisms including immune cell activation,pro-inflammatory cytokine secretion,and initiation of multiple signaling pathways.Excessive ECM deposition disrupts renal architecture and drives tubulointerstitial expansion,thereby accelerating renal functional decline.Recent studies demonstrate that chronic inflammation and fibrosis synergistically propagate DN progression via bidirectional crosstalk.Inflammation serves as an early driver of fibrogenesis and further amplifies fibrotic processes through positive feedback mechanisms,establishing a self-perpetuating inflammation-fibrosis vicious cycle.However,the precise molecular interplay between chronic inflammation and fibrosis remains incompletely elucidated.Thus,in-depth exploration of their interaction mechanisms is crucial for developing novel DN interventions.This review delineates the pathogenic roles of chronic inflammation and fibrosis in DN to advance mechanistic understanding and provide foundational insights for designing innovative therapeutic strategies.