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Recent advances in understanding the biochemical and molecular mechanism of diabetic nephropathy

机译:了解糖尿病肾病的生化和分子机制的最新进展

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Diabetic nephropathy (DN) is a chronic disease characterized by proteinuria, glomerular hypertrophy, decreased glomerular filtration and renal fibrosis with loss of renal function. DN is the leading cause of end-stage renal disease, accounting for millions of deaths worldwide. Hyperglycemia is the driving force for the development of diabetic nephropathy. The exact cause of diabetic nephropathy is unknown, but various postulated mechanisms are: hyperglycemia (causing hyperfiltration and renal injury), advanced glycosylation products, activation of cytokines. In this review article, we have discussed a number of diabetes-induced metabolites such as glucose, advanced glycation end products, protein kinase C and oxidative stress and other related factors that are implicated in the pathophysiology of the DN. An understanding of the biochemical and molecular changes especially early in the DN may lead to new and effective therapies towards prevention and amelioration of DN.
机译:糖尿病肾病(DN)是一种慢性疾病,其特征在于蛋白尿,肾小球肥大,肾小球滤过减少和肾纤维化,肾功能丧失。 DN是终末期肾脏疾病的主要原因,在全球范围内导致数百万人死亡。高血糖是糖尿病性肾病发展的驱动力。糖尿病肾病的确切原因尚不清楚,但各种推测的机制为:高血糖症(引起超滤和肾损伤),晚期糖基化产物,细胞因子激活。在这篇综述文章中,我们讨论了许多糖尿病诱导的代谢产物,例如葡萄糖,晚期糖基化终产物,蛋白激酶C和氧化应激以及与DN的病理生理有关的其他相关因素。对生化和分子变化(尤其是在DN早期)的了解可能会导致针对DN的预防和改善的新的有效疗法。

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