CD36 deficiency inhibits proliferation by cell cycle control in skeletal muscle cells

• DOI: 10.3389/fphys.2022.947325
• Publication Date: 2022-08-30T09:21:12Z
• Authors: Jingyu Sun; Yajuan Su; Yaning Xu; Duran Qin; Qianhui He; Haiping Qiu; Jiatong Zhuo; Weida Li
• Keywords: C2C12; CD36

Obesity-related muscular dysfunction and relative muscle atrophy affect an increasing number of people. Elucidating the molecular mechanisms skeletal cell development growth may contribute to maintenance mass in obesity. Fatty acid translocase (FAT/CD36), as a long-chain fatty transport protein, is crucial for lipid metabolism signaling. CD36 known function myogenic differentiation, whether it affects proliferation cells underlying remain unclear. In this study, effect deficiency on viability was examined using C2C12 myoblasts. Results showed that deletion enhanced inhibitory PA promotion apoptosis cells. Intriguingly, silencing suppressed by preventing cycle from G0/G1 phase S cyclin D1/CDK4-dependent manner. Overall, we demonstrated involved control, these findings might facilitate treatment obesity-related wasting.