The role of reactive oxygen species in apoptosis of the diabetic kidney.
until further notice
SourceApoptosis, 14, 12, (2009), pp. 1451-1458
Article / Letter to editor
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SubjectN4i 4: Auto-immunity, transplantation and immunotherapy; NCEBP 14: Cardiovascular diseases; NCMLS 1: Infection and autoimmunity; NCMLS 3: Tissue engineering and pathology; NCMLS 5: Membrane transport and intracellular motility
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.
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