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

Biochem Biophys Res Commun. 2013 Apr 19;433(4):359-61. doi: 10.1016/j.bbrc.2013.02.120. Epub 2013 Mar 26.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Cell Proliferation
  • Diabetic Nephropathies / physiopathology*
  • Enzyme Activation
  • Glycation End Products, Advanced / metabolism
  • Humans
  • Hyperglycemia / physiopathology*
  • Inflammation / physiopathology
  • Macrophages / metabolism
  • Oxidative Stress
  • PPAR gamma / metabolism
  • Protein Kinase C / metabolism
  • Reactive Oxygen Species / metabolism

Substances

  • Glycation End Products, Advanced
  • PPAR gamma
  • Reactive Oxygen Species
  • Protein Kinase C