Heart Aging Protein Found

Cardiovascular researchers working with a mouse model of the aging heart have identified a specific protein that contributes to deterioration of heart function and which may be a target for drug treatment to prevent or reverse the effects of aging on the heart muscle.

Investigators at the University of Alberta (Canada) focused on the protein CD36. CD36 is an integral membrane protein found on the surface of many cell types in vertebrate animals and is also known as FAT, SCARB3, GP88, glycoprotein IV (gpIV), and glycoprotein IIIb (gpIIIb). CD36 is a member of the class B scavenger receptor family of cell surface proteins. It binds many ligands including collagen, thrombospondin, erythrocytes parasitized with Plasmodium falciparum, oxidized low-density lipoprotein, native lipoproteins, oxidized phospholipids, and long-chain fatty acids. Recent work using genetically modified rodents have identified a clear role for CD36 in fatty acid and glucose metabolism, heart disease, taste, and dietary fat processing in the intestine.

In the current study published in the November 6, 2007, issue of Circulation, investigators genetically engineered a line of mice lacking CD36. When compared to normal mice, it was seen that the hearts of the CD36-deficient animals had lower levels of intramyocardial lipids, demonstrated improved mitochondria-derived ATP production, had significantly enhanced function, and had a blunted hypertrophic response.

The authors concluded that, "These findings provide evidence that CD36 mediates an age-induced cardiomyopathy in mice and suggest that inhibition of CD36 may be an approach for the treatment of the detrimental age-related effects on cardiac performance.”


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