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Diabetic nephropathy: an insight into molecular mechanisms and emerging therapies

机译：糖尿病肾病：深入了解分子机制和新疗法

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ABSTRACT Introduction: Diabetic kidney disease (DKD) is a major cause of morbidity and mortality in diabetes and is the most common cause of proteinuric and non-proteinuric forms of end-stage renal disease (ESRD). Control of risk factors such as blood glucose and blood pressure is not always achievable or effective. Significant research efforts have attempted to understand the pathophysiology of DKD and develop new therapies. Areas covered: We review DKD pathophysiology in the context of existing and emerging therapies that affect hemodynamic and metabolic pathways. Renin-angiotensin system (RAS) inhibition has become standard care. Recent evidence for renoprotective activity of SGLT2 inhibitors and GLP-1 agonists is an exciting step forward while endothelin receptor blockade shows promise. Multiple metabolic pathways of DKD have been evaluated with varying success; including mitochondrial function, reactive oxygen species, NADPH oxidase (NOX), transcription factors (NF-B and Nrf2), advanced glycation, protein kinase C (PKC), aldose reductase, JAK-STAT, autophagy, apoptosis-signaling kinase 1 (ASK1), fibrosis and epigenetics. Expert opinion: There have been major advances in the understanding and treatment of DKD. SGLT2i and GLP-1 agonists have demonstrated renoprotection, with novel therapies under evaluation. Addressing the interaction between hemodynamic and metabolic pathways may help achieve prevention, attenuation or even reversal of DKD.
机译：摘要介绍：糖尿病肾病（DKD）是糖尿病发病率和死亡率的主要原因，是终末期肾病（ESRD）的蛋白质和非蛋白质形式最常见的原因。控制血糖和血压等危险因素并不总是可实现的或有效的。重大的研究努力试图了解DKD的病理生理学，并开发新疗法。所涵盖的区域：我们在存在影响血液动力学和代谢途径的现有和新疗法的背景下审查DKD病理生理学。肾素 - 血管紧张素系统（RAS）抑制已成为标准护理。最近SGLT2抑制剂和GLP-1激动剂的初步证据是前进的令人兴奋的一步，而内皮素受体封锁显示承诺。 DKD的多种代谢途径已经通过不同的成功进行了评估;包括线粒体功能，反应性氧物种，NADPH氧化酶（NOx），转录因子（NF-B和NRF2），晚期糖化，蛋白激酶C（PKC），醛糖还原酶，JAK-STAT，自噬，凋亡 - 信号传导激酶1（Ask1 ），纤维化和表观生物学。专家意见：对DKD的理解和治疗有重大进展。 SGLT2i和GLP-1激动剂已经证明了RenoObotection，具有新的评估疗法。解决血液动力学和代谢途径之间的相互作用可能有助于实现预防，衰减甚至逆转DKD。

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