Acetyl-CoA Carboxylases and Diseases.
Level 5 - mechanism / opinion, no new human data
Narrative review of mechanisms and therapeutic targets without primary empirical data.
PubMed 35359351 · doi:10.3389/fonc.2022.836058
What was done
This narrative review summarizes literature on mammalian acetyl-CoA carboxylases (ACC1 and ACC2), focusing on their structural features, subcellular localization, regulatory mechanisms, functions in fatty acid synthesis and beta-oxidation, roles in protein post-translational modifications (acetylation and malonylation), associations with diseases like cancer, diabetes, and obesity, and the status of ACC1 inhibitors.
What was found
The abstract reports no quantitative data or specific numerical results. It outlines the biochemical roles of both isoforms: cytosolic ACC1 catalyzes the rate-limiting step in de novo fatty acid synthesis, whereas mitochondrial outer-membrane ACC2 generates malonyl-CoA to regulate carnitine palmitoyltransferase 1 (CPT1) in beta-oxidation. It also notes that manipulating acetyl-CoA and malonyl-CoA alters protein post-translational modification profiles.
Why it matters
The article provides a framework linking ACC-mediated lipid metabolism and downstream post-translational modifications to pathological processes, highlighting ACC1 as a potential drug target in oncology and metabolic disorders.
Limits
This is a non-systematic narrative review that introduces no primary experimental or clinical data. The abstract provides no search methodology, inclusion criteria, quality assessment of cited works, or quantitative metrics.
Cited by
- supports Transport of fatty acids into mitochondria for beta-oxidation via carnitine palmitoyltransferase (CPT) transporters is regulated by malonyl-CoA.