Fatty acid beta-oxidation enzyme (FAO enzyme (not specific, various common abbreviations exist for individual enzymes, e.g., ACAD, CPT1))

Fatty acid beta-oxidation enzymes are a group of mitochondrial and peroxisomal enzymes responsible for the stepwise breakdown of fatty acids into acetyl-CoA, NADH, and FADH₂, which are ultimately used for ATP production, particularly during fasting, exercise, or nutrient deprivation[1][2][3][6][7]. This process occurs mainly in the mitochondrial matrix and involves four core successive reactions: dehydrogenation by acyl-CoA dehydrogenase, hydration by enoyl-CoA hydratase, a second dehydrogenation by hydroxyacyl-CoA dehydrogenase, and thiolysis by 3-ketoacyl-CoA thiolase[2][3][5][6]. There are distinct enzyme isoforms specialized for short-, medium-, long-, and very-long-chain fatty acids[3]. The process is critical for energy homeostasis and is compromised in various inherited metabolic diseases and implicated in a range of pathologies including cancer, metabolic syndrome, and cardiovascular conditions[6][8]. Several clinically relevant inhibitors or modulators of FAO have been developed as experimental drugs, especially for metabolic, cardiovascular, and oncological indications[6]. Because "fatty acid oxidation enzymes" includes a family of targets, additional specificity is needed for precise therapeutic targeting.

Other names

Fatty acid oxidation enzymesFAO enzymesBeta-oxidation enzymes

Inhibition of specific FAO enzymes (e.g., CPT1) to limit fatty acid entry into mitochondria and suppress FAO - Stimulation of alternative energy metabolism pathways (e.g., shifting toward glucose oxidation in cardiac tissues) - Activation or upregulation of FAO to promote lipid catabolism