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首页> 外文期刊>Journal of cellular physiology. >Renoprotective mechanisms of sodium‐glucose co‐transporter 2 (SGLT2) inhibitors against the progression of diabetic kidney disease
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Renoprotective mechanisms of sodium‐glucose co‐transporter 2 (SGLT2) inhibitors against the progression of diabetic kidney disease

机译：Renoprotective机制的钠葡萄糖公司应承担的转运蛋白2 (SGLT2)抑制剂对糖尿病肾脏疾病的进展

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Abstract Sodium‐glucose co‐transporter 2 inhibitors (SGLT2‐Is) have emerged as a promising class of antidiabetic drugs with cardioprotective and renoprotective effects in patients with type 2 diabetes (T2D). The sodium‐glucose co‐transporters 1 and 2 (SGLT 1 and SGLT2) located in the renal proximal tubules are responsible for glucose reabsorption from the glomerular filtrate back into the systemic circulation. Inhibition of SGLT2, which accounts for about 90% of the glucose reabsorption, leads to a significant reduction in blood glucose levels and a concomitant increase in the urinary excretion of glucose (glycosuria). Multiple mechanisms contribute to the nephroprotective effects of SGLT2‐Is in T2D patients. These include: (1) Restoration of the tubuloglomerular feedback by increasing sodium delivery at macula densa, leading to afferent arteriolar constriction and reduced glomerular hyperfiltration, (2) Decreased activation of the intra‐renal renin‐angiotensin‐aldosterone system, which also contributes to reducing glomerular hyperfiltration, (3) Increased production of ketone bodies, which serves as an alternate fuel for adenosine triphosphate production in mitochondria, which helps in attenuating inflammation, and (4) Protection against hypoxia, oxidative stress, and fibrosis. This review elaborates on the key mechanisms that underlie the nephroprotective effects and the adverse effects of SGLT2‐Is in T2D patients with progressive diabetic kidney disease.
机译：文摘钠葡萄糖有限公司应承担的运输车2(SGLT2抑制剂所致)已经成为一种很有前途的与心血管类抗糖尿病的药物和renoprotective影响患者的类型2糖尿病(T2D)。公司应承担的转运蛋白1和2 (SGLT 1和SGLT2)位于肾近端小管负责葡萄糖重吸收的肾小球滤液回系统循环。大约90%的葡萄糖重吸收,线索在血糖显著降低水平,同时增加尿排泄的葡萄糖(糖尿)。有助于nephroprotective机制SGLT2在T2D应承担的病人的影响。包括:(1)tubuloglomerular的恢复反馈通过增加钠在黄斑交付densa,导致传入小动脉的收缩和减少肾小球反渗透法,(2)减少的激活这也有助于减少肾小球吗反渗透法,(3)增加生产酮体,作为替代燃料三磷酸腺苷生产线粒体,这有助于在衰减炎症,和(4)防止缺氧,氧化应激和纤维化。阐述了关键的背后机制nephroprotective影响和不利患者T2D SGLT2的影响量进步的糖尿病肾病。

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