摘要:
糖尿病肾病作为糖尿病最常见的并发症之一，是导致终末期肾病的主要原因。DN的发病机制包括慢性炎症、免疫细胞的募集与激活、肾小管与肾小球的损伤以及肾脏纤维化等过程，而这些过程与核苷酸结合寡聚化结构域样受体蛋白3（nucleotide-binding oligomerization domain-like receptor pyrin domain containing 3,NLRP3）炎症小体的激活及其所介导的细胞焦亡高度相关。既往研究表明，通过调控NLRP3炎症小体及其介导的细胞焦亡，可减少促炎性因子的释放、损伤相关分子模式（damage-associated molecular patterns,DAMPs）的泄漏、免疫细胞的募集和激活，进而减缓邻近细胞的炎症反应扩散、纤维化和组织重塑过程，并最终改善糖尿病肾病引起的肾脏损伤和功能障碍。本文进一步揭示NLRP3炎症小体及其介导的细胞焦亡在DN不同病理阶段中的分子调控机制，提出调控其激活的潜在靶点，为DN的个性化治疗提供了新方向。
Abstract:
Diabetic nephropathy (DN), as one of the most common complications of diabetes, is a primary cause of end-stage renal disease. The pathogenesis of DN encompasses processes such as chronic inflammation, recruitment and activation of immune cells, tubular and glomerular injury, and renal fibrosis. These processes are highly correlated with the activation of the nucleotide-binding oligomerization domain-like receptor pyrin domain containing 3 (NLRP3) inflammasome and the resulting pyroptosis it mediates. Previous studies have shown that the release of pro-inflammatory cytokines, leakage of damage-associated molecular patterns (DAMPs), recruitment and activation of immune cells can be reduced by regulating the NLRP3 inflammasome and its mediated pyroptosis, thereby slowing the diffusion of inflammatory responses in adjacent cells, fibrosis, and tissue remodeling processes. Ultimately, these process can improve renal injury and dysfunction caused by diabetic nephropathy. This article further elucidates the molecular regulatory mechanisms of the NLRP3 inflammasome and its mediated pyroptosis at different pathological stages of DN, proposes potential targets for regulating their activation, and provides a new direction for personalized treatment of DN.
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