Zoja Carlamaria, Xinaris Christodoulos, Macconi Daniela
Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Centro Anna Maria Astori, Science and Technology Park Kilometro Rosso, Bergamo, Italy.
University of Nicosia Medical School, Nicosia, Cyprus.
Front Pharmacol. 2020 Dec 21;11:586892. doi: 10.3389/fphar.2020.586892. eCollection 2020.
Diabetic nephropathy (DN) is one of the major microvascular complications of diabetes mellitus and the leading cause of end-stage kidney disease. The standard treatments for diabetic patients are glucose and blood pressure control, lipid lowering, and renin-angiotensin system blockade; however, these therapeutic approaches can provide only partial renoprotection if started late in the course of the disease. One major limitation in developing efficient therapies for DN is the complex pathobiology of the diabetic kidney, which undergoes a set of profound structural, metabolic and functional changes. Despite these difficulties, experimental models of diabetes have revealed promising therapeutic targets by identifying pathways that modulate key functions of podocytes and glomerular endothelial cells. In this review we will describe recent advances in the field, analyze key molecular pathways that contribute to the pathogenesis of the disease, and discuss how they could be modulated to prevent or reverse DN.
糖尿病肾病（DN）是糖尿病主要的微血管并发症之一，也是终末期肾病的主要病因。糖尿病患者的标准治疗方法包括控制血糖和血压、降低血脂以及阻断肾素 - 血管紧张素系统；然而，如果在疾病进程后期才开始这些治疗方法，它们只能提供部分肾脏保护作用。开发有效治疗DN的一个主要限制是糖尿病肾脏复杂的病理生物学特性，其会经历一系列深刻的结构、代谢和功能变化。尽管存在这些困难，但糖尿病实验模型通过识别调节足细胞和肾小球内皮细胞关键功能的途径，揭示了有前景的治疗靶点。在本综述中，我们将描述该领域的最新进展，分析导致该疾病发病机制的关键分子途径，并讨论如何调节这些途径以预防或逆转DN。
