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Diabetes

p53 is required for chloroquine-induced atheroprotection but not insulin sensitization

Author(s): 
Babak Razani, Chu Feng and Clay F. Semenkovich
Reference: 
J. Lipid Res., doi:10.1194/jlr.M003681
Contact email: 
csemenko@dom.wustl.edu

ATM, mutated in ataxia telangiectasia, is critical for the genotoxic stress response and its deficiency is associated with accelerated atherosclerosis and insulin resistance in humans and mice. The anti-malarial drug chloroquine activates ATM signaling and improves metabolic phenotypes in mice.

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