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CD36 actions in the heart: Lipids, calcium, inflammation, repair and more?
Nada A Abumrad1, Ira J Goldberg2
1Departments of Medicine and Cell Biology, Washington University, St. Louis, MO, United States..
Insights
CD36 receptor is crucial for heart fatty acid uptake and metabolism. Its absence impairs fatty acid utilization, impacting cardiac function and repair, highlighting its complex role in heart health.
Area of Science:
- Cardiovascular Biology
- Metabolic Regulation
- Immunology
Background:
- CD36 is a receptor involved in lipid metabolism and immune responses.
- Its role in myocardial fatty acid uptake is significant, affecting heart function.
- CD36 is expressed in both cardiac endothelial cells and cardiomyocytes.
Purpose of the Study:
- To review recent advancements in understanding CD36's multifaceted roles in the heart.
- To highlight key areas for future research on CD36 in cardiac metabolism and repair.
Main Methods:
- Literature review of studies on CD36 function in the heart.
- Analysis of CD36's impact on fatty acid uptake, signaling, and cellular processes.
- Examination of CD36's role in both normal physiology and pathological conditions.
Main Results:
- CD36 mediates high-affinity uptake of long-chain fatty acids in the heart.
- It regulates fatty acid utilization, AMPK activation, and phospholipid remodeling.
- CD36 contributes to lipid accumulation and inflammation under excess fatty acid supply but aids repair post-injury.
Conclusions:
- CD36 is a critical regulator of cardiac immuno-metabolism, influencing fatty acid handling and myocardial repair.
- Further investigation is needed to fully elucidate CD36's complex signaling pathways and therapeutic potential in heart disease.
Abstract:
CD36 is a multifunctional immuno-metabolic receptor with many ligands. One of its physiological functions in the heart is the high-affinity uptake of long-chain fatty acids (FAs) from albumin and triglyceride rich lipoproteins. CD36 deletion markedly reduces myocardial FA uptake in rodents and humans. The protein is expressed on endothelial cells and cardiomyocytes and at both sites is likely to contribute to FA uptake by the myocardium. CD36 also transduces intracellular signaling events that influence how the FA is utilized and mediate metabolic effects of FA in the heart. CD36 transduced signaling regulates AMPK activation in a way that adjusts oxidation to FA uptake. It also impacts remodeling of myocardial phospholipids and eicosanoid production, effects exerted via influencing intracellular calcium (iCa(2+)) and the activation of phospholipases. Under excessive FA supply CD36 contributes to lipid accumulation, inflammation and dysfunction. However, it is also important for myocardial repair after injury via its contribution to immune cell clearance of apoptotic cells. This review describes recent progress regarding the multiple actions of CD36 in the heart and highlights those areas requiring future investigation. This article is part of a Special Issue entitled: Heart Lipid Metabolism edited by G.D. Lopaschuk.
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