Dysregulation of CD36 and CPT1A is associated with fatty acid metabolic disorder and cardiomyocyte injury after high-cervical spinal cord injury.

To explore the expression changes of fatty acid translocase (CD36) and carnitine palmitoyltransferase 1a (CPT1A) in rat cardiomyocytes after high-cervical spinal cord injury (SCI), and to clarify their relationship with Fatty acid metabolism disturbance and acute myocardial damage. Thirty-six male Sprague-Dawley rats were randomly assigned to control, sham-operation, and high-cervical SCI groups. A C7 contusion model was established by a modified Allen weight-drop method, with SCI rats sampled at 4, 12, 24, and 48 h post-injury. Myocardial ultrastructure was examined by transmission electron microscopy. The GSE45006 spinal cord transcriptomic dataset was reanalyzed for Cd36 and Cpt1a expression at 1 and 3 days after SCI. Cd36 mRNA and CPT1A protein levels in cardiac tissue were quantified by qRT-PCR and Western blotting, respectively. TEM showed progressively worsening myocardial ultrastructural injury in SCI rats from 4 to 48 h, manifesting as mitochondrial swelling, myofilament disarray, and intracellular edema. Bioinformatics analysis of injured spinal cord tissue showed that Cd36 was significantly upregulated at both 1 and 3 days after SCI, whereas Cpt1a was upregulated at 1 day and returned toward the sham level by 3 days. In cardiac tissue, Cd36 mRNA was significantly elevated at 4 h and reduced at 48 h, and CPT1A protein showed a parallel biphasic trend over the same period in the SCI group. No significant differences were detected between the control and sham groups. Dynamic dysregulation of CD36/CPT1A is associated with myocardial fatty acid metabolic disturbance after high-cervical SCI and may be involved in acute myocardial injury. CD36 and CPT1A may serve as potential targets for the prevention and treatment of SCI-induced myocardial dysfunction.