by Emily Poulin
Atherosclerosis, a leading cause of heart attack and stroke, is characterized by a buildup of debris in artery walls, called plaques. Macrophages, a type of white blood cell, are important cellular factors in atherosclerotic plaque development and are known to affect the severity of the disease.
Akt, a signaling protein important for macrophage survival and inflammatory response, has three forms that differentially affect plaque establishment and severity. In the Journal of Lipid Research, Vladimir Babaev, M.D., Ph.D., MacRae Linton, M.D., and colleagues report that Akt2 deletion in macrophages dramatically decreases plaque formation in a mouse model of atherosclerosis.
The researchers report that deletion of Akt2, but not Akt1, in macrophages resulted in smaller plaques that contained fewer macrophages. The macrophages present in mice lacking macrophage Akt2 were largely of the anti-inflammatory M2 subtype that is associated with reduced macrophage recruitment to plaques.
The findings demonstrate that Akt2 critically influences macrophage biology during atherosclerotic plaque development, supporting Akt2 signaling as an important therapeutic target for the prevention of cardiovascular disease.
This study was supported by National Institutes of Health grants HL105375, DK050435, DK059637 and HL116263.
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