This study investigates the role of FUNDC1 in protecting spinal cord neurons against ischemic injury. FUNDC1, a mitophagy receptor, was found to enhance mitophagy and inhibit mitochondria-dependent apoptosis in the early stages of spinal cord injury (SCI). In a rat SCI model, overexpression of FUNDC1 using AAV-D1 improved locomotor recovery, reduced neuronal apoptosis, and preserved spinal cord structure. In vitro studies using an oxygen-glucose deprivation (OGD) model showed that FUNDC1 enhanced mitophagy, reduced mitochondrial damage, and improved mitochondrial function. The protective effects of FUNDC1 were mediated through mitophagy, as demonstrated by the reversal of these effects by the autophagy inhibitor 3-methyladenine (3-MA). These findings suggest that FUNDC1 can be a potential therapeutic target for early intervention in SCI by enhancing mitophagy and protecting against neuronal loss.This study investigates the role of FUNDC1 in protecting spinal cord neurons against ischemic injury. FUNDC1, a mitophagy receptor, was found to enhance mitophagy and inhibit mitochondria-dependent apoptosis in the early stages of spinal cord injury (SCI). In a rat SCI model, overexpression of FUNDC1 using AAV-D1 improved locomotor recovery, reduced neuronal apoptosis, and preserved spinal cord structure. In vitro studies using an oxygen-glucose deprivation (OGD) model showed that FUNDC1 enhanced mitophagy, reduced mitochondrial damage, and improved mitochondrial function. The protective effects of FUNDC1 were mediated through mitophagy, as demonstrated by the reversal of these effects by the autophagy inhibitor 3-methyladenine (3-MA). These findings suggest that FUNDC1 can be a potential therapeutic target for early intervention in SCI by enhancing mitophagy and protecting against neuronal loss.