[Molecular mechanism of diabetic nephropathy].

Abstract

Diabetic nephropathy(DN) is the most common cause of end-stage renal disease, and is characterized by excessive accumulation of extracellular matrix in the kidney. Chronic hyperglycemia is the main cause of DN. Multiple theories have been proposed to explain the adverse effect of hyperglycemia, including an increased flux through the polyol pathway, excessive formation of advanced glycation end-products, oxidative stress, and activation of the protein kinase C (PKC) pathway. In this article, we review evidence that supports these theories, and focus our attention on the PKC theory. Therapeutic interventions to inhibit PKC are effective in reducing DN in diabetic animals. Currently, clinical trials are in progress to determine the efficacy of a PKC beta inhibitor for the treatment of diabetic complications including DN. PKC beta inhibitors may be included as a first line treatment for DN in a near future.

• Authors: Yuzuru Ohshiro, Nobuyuki Takasu
• Journal: Nihon rinsho. Japanese journal of clinical medicine (Nihon Rinsho) Vol. 64 Issue 5 Pg. 997-1003 (May 2006) ISSN: 0047-1852 [Print] Japan
• PMID: 16689387 (Publication Type: English Abstract, Journal Article, Review)

Chemical References

• Proto-Oncogene Proteins c-akt

Topics

• Animals
• Diabetic Nephropathies (drug therapy, metabolism)
• Proto-Oncogene Proteins c-akt (antagonists & inhibitors)