The role of reactive oxygen species in apoptosis of the diabetic kidney.
Increased levels of reactive oxygen species (ROS) by hyperglycemia can induce apoptosis of renal cells and diabetic nephropathy. The redox balance in the renal cell seems, therefore, of the utmost importance. ROS-mediated apoptosis may be further aggravated by an inadequate cytoprotective response against ROS. When there are insufficient cytoprotective and ROS scavenging molecules, ROS lead to considerable cellular damage and to a point of no return in apoptosis. Induction of cytoprotective proteins may prevent or attenuate apoptosis, renal cell injury, and finally diabetic nephropathy. Here, we discuss some mechanisms of apoptosis and several strategies that have been probed to ameliorate, or to prevent apoptosis in the diabetic kidney.
Wagener
F A D T G
FA
Department of Pharmacology and Toxicology, Nijmegen Centre for Molecular Life Sciences, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands. f.wagener@ncmls.ru.nl
Dekker
D
D
Berden
J H
JH
Scharstuhl
A
A
van der Vlag
J
J
D000818:Animals; D017209:Apoptosis; D003928:Diabetic Nephropathies / Q000378:metabolism / Q000503:physiopathology* / Q000517:prevention & control; D006801:Humans; D007668:Kidney / Q000166:cytology* / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism*
D017382:Reactive Oxygen Species