Fig. 9.

Schematic diagram of the involvement of FABP3 and FABP5 in mitochondria-associated apoptosis pathways in ischemic neurons. FABP3 and FABP5 have similar mechanisms of action. These proteins exacerbate oxidative stress injury by mediating the accumulation of 4-HNE, a toxic byproduct of fatty acid peroxidation. FABP3/5 are also involved in mitochondrial BAX and VDAC channel formation, which reduces the mitochondrial membrane potential and results in apoptotic signaling. The FABP3/5 inhibitor HY08 effectively inhibits FABP function, helps mitochondria to resist ischemic damage, and enhances neuronal tolerance to ischemia. Thus, HY08 protects against mitochondrial damage and is a potential treatment for ischemic stroke.