ArticleFrontiers in physiology2022
CD36 deficiency inhibits proliferation by cell cycle control in skeletal muscle cells.
Article in Frontiers in physiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- PPARα-CD36-CAV1-mediated docosahexaenoic acid (DHA) uptake promotes muscle fiber development in grass carp (Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2026Article
- Integrative transcriptomics defines CD36 as a key regulator of immunometabolic signaling in acute myeloid leukemia.Genes & genomics · 2026Article
- Transcriptome analysis reveals the regulatory mechanism of myofiber development in male and female black Muscovy duck at different ages.Frontiers in veterinary science · 2024Article
- Article
- Differential Roles of CD36 in Regulating Muscle Insulin Response Depend on Palmitic Acid Load.Biomedicines · 2023Article
- Co-Expression Transcriptomic Profiling Identifies Sex-Universal Molecular Markers of Muscle Atrophy.IET systems biologyArticle
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Obesity-related muscular dysfunction and relative muscle atrophy affect an increasing number of people. Elucidating the molecular mechanisms of skeletal muscle cell development and growth may contribute to the maintenance of skeletal muscle mass in obesity. Fatty acid translocase (FAT/CD36), as a long-chain fatty acid transport protein, is crucial for lipid metabolism and signaling. CD36 is known to function in myogenic differentiation, and whether it affects the proliferation of skeletal muscle cells and the underlying mechanisms remain unclear. In this study, the effect of CD36 deficiency on skeletal muscle cell viability and proliferation was examined using C2C12 myoblasts. Results showed that the deletion of CD36 enhanced the inhibitory effect of PA on the proliferation and the promotion of apoptosis in skeletal muscle cells. Intriguingly, the silencing of CD36 suppressed cell proliferation by preventing the cell cycle from the G0/G1 phase to the S phase in a cyclin D1/CDK4-dependent manner. Overall, we demonstrated that CD36 was involved in skeletal muscle cell proliferation by cell cycle control, and these findings might facilitate the treatment of obesity-related muscle wasting.
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