Objective · To investigate the effects and potential mechanisms of fatty acid binding protein 3 (FABP3) on cell survival under hypoxia. Methods · Neonatal rat ventricular myocytes were stimulated with recombinant human FABP3 proteins, and then the differences of cell viability and cell death between groups were verifiedtrypan blue assay and MTT assay. Besides, the of PARP and caspase 3 protein, the level of reactive oxygen species (ROS), and mitochondrial membrane potentials under hypoxia were compared between groups for more confirmation. Results · FABP3 increased cardiomyocytes’ death and decreased cell viability under hypoxia (P0.021). It was discovered that FABP3 upregulated the levels of cleaved PARP and cleaved caspase 3 (P0.006, P0.002), increased the level of intracellular ROS (P0.038), and declined the mitochondrial membrane potentials as well (P0.002). Conclusion · FABP3 contributes to cell survival and apoptosisregulating intracellular ROS and mitochondrial membrane potentials under hypoxia.