A kidney perspective on the mechanism of action of sodium glucose co-transporter 2 inhibitors

被引:100
作者
Sen, Taha [1 ]
Heerspink, Hiddo J. L. [1 ,2 ]
机构
[1] Univ Groningen, Univ Med Ctr Groningen, Dept Clin Pharm & Pharmacol, Groningen, Netherlands
[2] George Inst Global Hlth, Sydney, NSW, Australia
关键词
SGLT2; INHIBITION; KETONE-BODY; URIC-ACID; CARDIOVASCULAR OUTCOMES; ARTERIAL STIFFNESS; NLRP3; INFLAMMASOME; OXIDATIVE STRESS; BLOOD-PRESSURE; CANAGLIFLOZIN; EMPAGLIFLOZIN;
D O I
10.1016/j.cmet.2021.02.016
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Sodium glucose co-transporter (SGLT) 2 inhibitors reduce the risk of kidney failure in patients with and without type 2 diabetes (T2D). Although the precise underlying mechanisms for these nephroprotective effects are incompletely understood, various hypotheses have been proposed including reductions in intraglomerular pressure through restoration of tubuloglomerular feedback, blood pressure reduction and favorable effects on vascular function, reduction in tubular workload and hypoxia, and metabolic effects resulting in increased autophagy. Here, we review these mechanisms, which may also explain the beneficial effects of SGLT2 inhibitors on kidney function in patients without T2D.
引用
收藏
页码:732 / 739
页数:8
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