What question did this study set out to answer?

This research aims to investigate the role of CD36 in lipotoxic cardiomyopathy in mice with cardiac-restricted PPARalpha overexpression.

March 16, 2007Circulation ResearchOpen Access

CD36 Deficiency Rescues Lipotoxic Cardiomyopathy

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Why the study?

Does CD36 deficiency prevent lipotoxic cardiomyopathy in MHC-PPARalpha mice?

Population

Mice with cardiac-restricted overexpression of PPARalpha (MHC-PPARalpha mice)

Comparison

CD36 deficiency (MHC-PPARalpha/CD36-/- mice) vs MHC-PPARalpha mice with intact CD36

Design

Preclinical

Authors

JYJohn YangTufts Medical Center NSNandakumar SambandamSanford Burnham Prebys Medical Discovery Institute XHXianlin HanZhejiang Chinese Medical University

Discussion

Member takes

Implication

CD36 merits exploration as a therapeutic target in lipotoxic cardiomyopathy; this animal finding leaves clinical translation open.

Key Points

This research aims to investigate the role of CD36 in lipotoxic cardiomyopathy in mice with cardiac-restricted PPARalpha overexpression.
MHC-PPARalpha mice were crossed with CD36-deficient mice to study the effects on cardiac dysfunction and lipid metabolism.
High-fat diet administration was used to assess the influence of CD36 deficiency on metabolic abnormalities.
CD36 deficiency prevented myocyte triacylglyceride accumulation and cardiac dysfunction in MHC-PPARalpha mice.
Increased glucose uptake and oxidation were observed in CD36-deficient mice, despite unchanged FA oxidation pathways.
Reversal of PPARalpha-mediated suppression of glucose uptake and oxidation genes occurred in MHC-PPARalpha/CD36-/- mice.

Structured PICO

Does CD36 deficiency prevent lipotoxic cardiomyopathy in MHC-PPARalpha mice?

Population

Mice with cardiac-restricted overexpression of PPARalpha (MHC-PPARalpha mice)

Intervention

CD36 deficiency (MHC-PPARalpha/CD36-/- mice)

Comparator

MHC-PPARalpha mice with intact CD36

Outcome

Myocyte triacylglyceride accumulation and cardiac dysfunctionsurrogate

CD36 deficiency rescues lipotoxic cardiomyopathy in a mouse model of cardiac-restricted PPARalpha overexpression by restoring glucose uptake and oxidation.

Cite This Study

Yang et al. (2007) studied this question.

synapsesocial.com/papers/69fd29dc30a474415f89e2da https://doi.org/10.1161/01.res.0000264104.25265.b6

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CD36 Deficiency Rescues Lipotoxic Cardiomyopathy

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

CD36 Deficiency Rescues Lipotoxic Cardiomyopathy

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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