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World J Diabetes. Apr 15, 2013; 4(2): 27-30
Published online Apr 15, 2013. doi: 10.4239/wjd.v4.i2.27
Diabetes and renal tubular cell apoptosis
Samy L Habib
Samy L Habib, South Texas Veterans Health Care System, Departments of Cellular and Structural Biology, University of Texas Health Science Center, San Antonio, TX 78229, United States
Author contributions: Habib SL solely contributed to this article.
Supported by Grants from the American Heart Association, to Habib SL
Correspondence to: Samy L Habib, MS, PhD, Associate Professor, South Texas Veterans Health Care System, Departments of Cellular and Structural Biology, University of Texas Health Science Center, 7703 Floyd Curl Dr., San Antonio, TX 78229, United States. habib@uthscsa.edu
Telephone: +1-210-5673816 Fax: +1-210-5673802
Received: January 10, 2012
Revised: March 26, 2013
Accepted: March 28, 2013
Published online: April 15, 2013
Processing time: 95 Days and 18.3 Hours
Abstract

Apoptosis contributes to the development of diabetic nephropathy, but the mechanism by which high glucose induces apoptosis is not fully understood. Apoptosis of tubular epithelial cells is a major feature of diabetic kidney disease, and hyperglycemia triggers the generation of free radicals and oxidant stress in tubular cells. Hyperglycemia and high glucose in vitro also lead to apoptosis, a form of programmed cell death. High glucose similar to those seen with hyperglycemia in people with diabetes mellitus, lead to accelerated apoptosis, a form of programmed cell death characterized by cell shrinkage, chromatin condensation and DNA fragmentation, in variety of cell types, including renal proximal tubular epithelial cells.

Keywords: Tubular cells; Renal; Apoptosis; Diabetes

Core tip: Apoptosis contributes to the development of diabetic nephropathy, but the mechanism by which high glucose induces apoptosis is not fully understood. High glucose similar to those seen with hyperglycemia in people with diabetes mellitus, lead to accelerated apoptosis, a form of programmed cell death characterized by cell shrinkage, chromatin condensation and DNA fragmentation, in variety of cell types, including renal proximal tubular epithelial cells.