2024 | Dehui Chen, Linguan Zhou, Gang Chen, Taotao Lin, Jiemin Lin, Xin Zhao, Wenwen Li, Shengyu Guo, Rongcan Wu, Zhenyu Wang and Wenge Liu
FUNDC1 induces mitophagy to protect spinal cord neurons against ischemic injury. This study demonstrates that overexpression of FUNDC1 enhances mitophagy and reduces neuronal apoptosis in spinal cord injury (SCI). In a rat SCI model, FUNDC1 overexpression increased neuronal autophagy and decreased apoptosis, reducing spinal cord damage. In vitro studies showed that FUNDC1 inhibited mitochondria-dependent apoptosis and improved mitochondrial function. FUNDC1 also enhanced mitophagy, and its protective effects were reversed by the autophagy inhibitor 3-MA. These findings suggest that FUNDC1 protects against neuronal loss after SCI by inducing mitophagy, inhibiting mitochondrial apoptosis, and improving mitochondrial function. The study also shows that FUNDC1 overexpression enhances autophagy and reduces apoptosis in the SCI model and in an in vitro oxygen-glucose deprivation (OGD) model. FUNDC1 modulates mitochondrial function and apoptosis by mediating mitophagy. The protective effects of FUNDC1 against apoptosis and mitochondrial dysfunction were mediated through mitophagy. These results indicate that FUNDC1 can be a target for early treatment of SCI.FUNDC1 induces mitophagy to protect spinal cord neurons against ischemic injury. This study demonstrates that overexpression of FUNDC1 enhances mitophagy and reduces neuronal apoptosis in spinal cord injury (SCI). In a rat SCI model, FUNDC1 overexpression increased neuronal autophagy and decreased apoptosis, reducing spinal cord damage. In vitro studies showed that FUNDC1 inhibited mitochondria-dependent apoptosis and improved mitochondrial function. FUNDC1 also enhanced mitophagy, and its protective effects were reversed by the autophagy inhibitor 3-MA. These findings suggest that FUNDC1 protects against neuronal loss after SCI by inducing mitophagy, inhibiting mitochondrial apoptosis, and improving mitochondrial function. The study also shows that FUNDC1 overexpression enhances autophagy and reduces apoptosis in the SCI model and in an in vitro oxygen-glucose deprivation (OGD) model. FUNDC1 modulates mitochondrial function and apoptosis by mediating mitophagy. The protective effects of FUNDC1 against apoptosis and mitochondrial dysfunction were mediated through mitophagy. These results indicate that FUNDC1 can be a target for early treatment of SCI.