A Compressive Review on Novel Molecular Target of Diabetic Nephropathy

Abstract

Diabetic nephropathy (DN) is a leading cause of mortality and morbidity, decreases quality of life and shortened life expectancy. The renin angiotensin system is considered to be involved in most of the pathological processes that result in diabetic nephropathy. Various subsystems of RAAS contribute to the disease pathology. One of these involves angiotensin II (Ang II) which shows increased activity during diabetic nephropathy. Evidence indicates interaction between advanced glycation end products (AGEs), activated protein kinase C (PKC) and angiotensin II provoke the progression of DN. Inhibitors of angiotensin-converting enzyme (ACEIs), renin angiotensin aldosterone system (RAAS), AGEs, and PKC have been tested for slowing down the progression of DN. This review focuses on the latest published data dealing with the pathophysiology, stages of DN, pathogenesis, prevention and treatment of DN.