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Protecting Against Oxidized Lipids
Excessive blood concentrations of oxidized cholesterol lead to the development of fatty plaques in blood vessels, a process called atherosclerosis. Blockage of blood vessels by fragments of ruptured plaques can lead to heart attacks, a major cause of mortality in developed nations. Mice that cannot efficiently clear lipoprotein-bound cholesterol from the bloodstream are a model for spontaneous atherosclerosis-induced myocardial infarctions. Kerr et al. found that the kinase Akt1 was activated in these mice, which was associated with accumulation of oxidized lipids. Deletion of the gene encoding Akt1 in these mice improved survival, reduced the severity of various cardiovascular complications, and decreased the incidence of spontaneous myocardial infarctions. Thus, using clinically available Akt inhibitors to normalize Akt activity could help to decrease some of the pathological effects that result from excessive lipid oxidation and atherosclerosis.
