On this basis, FAO mediates the entry of fatty acids into mitochondria via CPT1α, which is subsequently converted to acetyl-coenzyme A (acetyl-CoA) through a multi-step enzymatic reaction, and enters the tricarboxylic acid (TCA) cycle to generate ATP, and the enhancement of the activity or expression of CPT1 can effectively attenuate renal fibrosis, suggesting that it may be a potential drug target for improving renal function (Lin et al., 2022). Here, CPT1A is linked to renal fibrosis.