Fabp3, also known as fatty acid binding protein 3 (muscle and heart), is a cytoplasmic fatty acid binding protein expressed in a tissue-specific manner, predominantly in breast, muscle, and heart. It is involved in various biological processes such as lipid metabolism and transport. By binding fatty acids, it may play a role in intracellular trafficking of lipids, which is crucial for normal cellular function and energy homeostasis [3].

In aged skeletal muscles, FABP3 is upregulated, disrupting homeostasis via lipid remodeling. FABP3 overexpression in young muscles mimics the aged-muscle lipid composition, causing ER stress through the PERK-eIF2α pathway and inhibiting protein synthesis, while FABP3 knockdown in aged muscles reduces ER stress and improves muscle recovery [1].

In mesenchymal stem cells, FABP3 promotes adipogenesis and inhibits osteogenesis. Knockdown of FABP3 alleviates bone loss in aged mice, indicating its role in the bone-fat balance during aging [2].

In the context of cerebral ischemia-reperfusion injury, FABP3 silencing in mice mitigates brain tissue damage, reduces infarct volume ratio, and attenuates neuronal apoptosis, as FABP3 activates mitochondrial autophagy through ROS, leading to mitochondrial dysfunction and neuronal apoptosis [4].

In conclusion, Fabp3 plays essential roles in multiple biological processes, including muscle homeostasis during aging, mesenchymal stem cell fate determination, and the progression of cerebral ischemia-reperfusion injury. The use of gene knockout models in these studies has provided valuable insights into the functions of Fabp3 in these specific disease-related biological processes, highlighting its potential as a therapeutic target for sarcopenia, senile osteoporosis, and stroke-related brain injury.