CD36 expression contributes to age-induced cardiomyopathy in mice.
BACKGROUND
Cardiac remodeling and impaired cardiac performance in the elderly significantly increase the risk of developing heart disease. Although vascular abnormalities associated with aging contribute to the age-related decline in cardiac function, myocardium-specific events may also be involved.


RESULTS
We show that intramyocardial lipid accumulation, as well as a reduction in both fatty acid and glucose oxidation and a subsequent deterioration in cardiac ATP supply, also occurs in aged mice. Consistent with an energetically compromised heart, hearts from aged mice display depressed myocardial performance and cardiac hypertrophy. Associated with this is a dramatic increase in the fatty acid transport protein CD36 in aged hearts compared with young hearts, which suggests that CD36 is a mediator of these multiple metabolic, functional, and structural alterations in the aged heart. In accordance with this, hearts from aged CD36-deficient mice have lower levels of intramyocardial lipids, demonstrate improved mitochondria-derived ATP production, have significantly enhanced function compared with aged wild-type mice, and have a blunted hypertrophic response.


CONCLUSIONS
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.
Koonen
Debby P Y
DP
Cardiovascular Research Group, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, Alberta, Canada T6G 2S2.
Febbraio
Maria
M
Bonnet
Sebastien
S
Nagendran
Jayan
J
Young
Martin E
ME
Michelakis
Evangelos D
ED
Dyck
Jason R B
JR
D000255:Adenosine Triphosphate / Q000378:metabolism; D000375:Aging / Q000502:physiology*; D000818:Animals; D018955:CD36 Antigens / Q000235:genetics* / Q000378:metabolism*; D009202:Cardiomyopathies / Q000378:metabolism* / Q000503:physiopathology*; D004734:Energy Metabolism / Q000502:physiology; D006321:Heart / Q000502:physiology; D006334:Heart Function Tests; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009206:Myocardium / Q000378:metabolism; D020257:Ventricular Remodeling / Q000502:physiology
D018955:CD36 Antigens; D000255:Adenosine Triphosphate