SGLT2 抑制剂和 NLRP3 炎症小体:糖尿病肾病的潜在靶点。

IF 1.3 Q3 UROLOGY & NEPHROLOGY
Paulo André Bispo Machado Júnior, André Lass, Bruna Isadora Pilger, Raphaella Fornazari, Thyago Proença de Moraes, Ricardo Aurino Pinho
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引用次数: 0

摘要

糖尿病肾病(DKD)仍然是全球慢性肾病(CKD)的主要病因。DKD 的发病机制受功能、组织病理学和免疫机制的影响,包括 NLRP3 炎性体活性和氧化应激。多年来,钠-葡萄糖共转运体 2 抑制剂(SGLT2i)已在多项临床研究中显示出其代谢优势和减缓 DKD 病程进展的能力。最近的研究表明,其抗糖尿病活性还延伸到抑制炎症反应,包括调节 NLRP3 炎性体、减少促炎症标志物和减少氧化应激。在此,我们回顾了 SGLT2i 治疗慢性肾脏病的疗效,并讨论了炎症反应在慢性肾脏病发展中的作用,包括其与 NLRP3 炎症小体和氧化应激的关系。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
SGLT2 inhibitors and NLRP3 inflammasome: potential target in diabetic kidney disease.

Diabetic kidney disease (DKD) remains the leading cause of chronic kidney disease (CKD) worldwide. The pathogenesis of DKD is influenced by functional, histopathological, and immune mechanisms, including NLRP3 inflammasome activity and oxidative stress. The sodium-glucose cotransporter 2 inhibitors (SGLT2i) have shown metabolic benefits and the ability to slow the progression of DKD in several clinical studies over the years. Recent studies suggest that the antidiabetic activity also extends to inhibition of the inflammatory response, including modulation of the NLRP3 inflammasome, reduction of pro-inflammatory markers and reduction of oxidative stress. Here we review the efficacy of SGLT2i in the treatment of CKD and discuss the role of the inflammatory response in the development of DKD, including its relationship to the NLRP3 inflammasome and oxidative stress.

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来源期刊
CiteScore
2.20
自引率
16.70%
发文量
208
审稿时长
16 weeks
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