What question did this study set out to answer?

To review the contradictory roles of scavenger receptor CD36 in lipid homeostasis and determine how its expression influences the development of atherosclerosis.

February 26, 2018British Medical BulletinOpen Access

CD36 and lipid metabolism in the evolution of atherosclerosis

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Authors

LZLei ZhaoZunyi Medical University ZVZac VargheseThe Royal Free Hospital JMJ.F. MoorheadMinnesota State University Moorhead

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Implication

Literature review uncovers paradoxical atherogenic effects from both CD36 elevation and deficiency in vascular models, suggesting an optimal therapeutic window of expression.

Key Points

To review the contradictory roles of scavenger receptor CD36 in lipid homeostasis and determine how its expression influences the development of atherosclerosis.
Narrative review synthesizing academic literature on CD36 receptor biology, lipid transport, and atherogenesis.
Pathological upregulation of CD36 accelerates atherosclerosis by inducing endothelial apoptosis, foam cell formation, macrophage trapping, vascular inflammation, and thrombosis.
CD36 deficiency also promotes atherosclerotic risk by triggering dyslipidemia, subclinical systemic inflammation, and metabolic disorders.
Evidence points toward an optimal protective window of CD36 expression, indicating that post-translational modulation represents a viable alternative to total gene inhibition or overexpression.

Cite This Study

Zhao et al. (2018) studied this question.

synapsesocial.com/papers/6a174a1895fbca339c8d8131 https://doi.org/10.1093/bmb/ldy006

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Implication

Literature review uncovers paradoxical atherogenic effects from both CD36 elevation and deficiency in vascular models, suggesting an optimal therapeutic window of expression.

CD36 and lipid metabolism in the evolution of atherosclerosis

Discussion

Member takes

Implication

Key Points

Cite This Study

CD36 and lipid metabolism in the evolution of atherosclerosis

Discussion

Member takes

Implication

Key Points

Cite This Study

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