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Fatty acid β-oxidation pathway enzymes are a set of mitochondrial (and peroxisomal) enzymes that catalyze the stepwise removal of two-carbon units from fatty acids, generating acetyl-CoA, NADH, and FADH2 for energy production[2][3][4]. The main steps in mitochondrial β-oxidation are catalyzed by acyl-CoA dehydrogenase, enoyl-CoA hydratase, 3-hydroxyacyl-CoA dehydrogenase, and β-ketothiolase. These enzymes have isoforms with different specificity for fatty acid chain length. Dysfunction in any of these enzymes can lead to serious metabolic disorders. Some pharmacological agents modulate this pathway for therapeutic benefit, but inhibition or overactivation may be associated with adverse outcomes[2][4]. Note: This entry represents a pathway/functional enzyme group, not a single molecule, which is why using it as a canonical target is technically incorrect. For structured data, listing the individual main enzymes (e.g., "Acyl-CoA dehydrogenase (ACAD)", "Enoyl-CoA hydratase", etc.) is preferred[4][2][3].
Inhibition of fatty acid import into mitochondria (e.g., CPT1 inhibition) Enhancement (upregulation) of enzyme gene expression (via PPAR activation) Cofactor supplementation (riboflavin) Metabolic modulation (e.g., reducing fatty acid oxidation in heart failure)
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