Platelet Acetyl-CoA Carboxylase Phosphorylation: A Risk Stratification Marker That Reveals Platelet-Lipid Interplay in Coronary Artery Disease Patients

JACC Basic Transl Sci. 2019 Sep 11;4(5):596-610. doi: 10.1016/j.jacbts.2019.04.005. eCollection 2019 Sep.

Abstract

Adenosine monophosphate-activated protein kinase (AMPK) acetyl-CoA carboxylase (ACC) signaling is activated in platelets by atherogenic lipids, particularly by oxidized low-density lipoproteins, through a CD36-dependent pathway. More interestingly, increased platelet AMPK-induced ACC phosphorylation is associated with the severity of coronary artery calcification as well as acute coronary events in coronary artery disease patients. Therefore, AMPK-induced ACC phosphorylation is a potential marker for risk stratification in suspected coronary artery disease patients. The inhibition of ACC resulting from its phosphorylation impacts platelet lipid content by down-regulating triglycerides, which in turn may affect platelet function.

Keywords: ACC, acetyl-CoA carboxylase; AMPK; AMPK, adenosine monophosphate–activated protein kinase; AU, arbitrary units; AoC, extra-coronary calcification score; CAC, coronary artery calcification; CAD, coronary artery disease; S-CAD, stable coronary artery disease; TG, triglyceride; acetyl-CoA carboxylase; coronary artery disease; lipidomics; oxLDL, oxidized low-density lipoprotein; phosphoACC, acetyl-CoA carboxylase phosphorylation on serine 79; platelet.