Kidney Disease in Diabetes Mellitus: Cross-Linking between Hyperglycemia, Redox Imbalance and Inflammation
Kidney Disease in Diabetes Mellitus: Cross-Linking between Hyperglycemia, Redox Imbalance and Inflammation
复制标题
DOI：
10.5935/abc.20190077
复制
发表时间：
2019-05-01
影响因子：
2.6
通讯作者：
Santos, Juliana Célia de Farias
中科院分区：
文献类型：
--
作者：
Amorim, Rayne Gomes;Guedes, Glaucevane da Silva;Santos, Juliana Célia de Farias
慢性高血糖是糖尿病大血管和微血管并发症的关键。高糖导致氧化还原失衡和全身及肾内炎症，在糖尿病肾病的发病机制中起着关键作用，糖尿病肾病是目前世界上导致透析的主要原因。该病的发病机制复杂、多因素且尚未完全阐明，许多因素和机制参与了该病的发生、发展和临床转归。尽管与糖尿病相关的肾脏损害的机制不同，但涉及氧化/炎症途径的代谢机制已被广泛接受。这是慢性高血糖状态触发氧化应激和炎症的明显证据，氧化应激和炎症是通过改变代谢途径在自我延续的循环中介导的，促进细胞损伤和终末期肾脏疾病的进展。本研究介绍了糖尿病肾病发病机制中氧化还原失衡和慢性高血糖所致炎症的代谢途径的最新进展。
Chronic hyperglycemia is the key point of macro- and microvascular complications associated with diabetes mellitus. Excess glucose is responsible for inducing redox imbalance and both systemic and intrarenal inflammation, playing a critical role in the pathogenesis of diabetic kidney disease, which is currently the leading cause of dialysis in the world. The pathogenesis of the disease is complex, multifactorial and not fully elucidated; many factors and mechanisms are involved in the development, progression and clinical outcomes of the disease. Despite the disparate mechanisms involved in renal damage related to diabetes mellitus, the metabolic mechanisms involving oxidative/inflammatory pathways are widely accepted. The is clear evidence that a chronic hyperglycemic state triggers oxidative stress and inflammation mediated by altered metabolic pathways in a self-perpetuating cycle, promoting progression of cell injury and of end-stage renal disease. The present study presents an update on metabolic pathways that involve redox imbalance and inflammation induced by chronic exposure to hyperglycemia in the pathogenesis of diabetic kidney disease.