Apolipoprotein C3 (apoC3) is a triglyceride-rich lipoprotein–associated protein known to promote hyperlipidemia, inflammation, and atherosclerosis, and is strongly linked to cardiovascular risk.

Our new study, published in the Journal of Thrombosis and Haemostasis, uncovers an unexpected counter-effect: apoC3 directly suppresses platelet activation and aggregation. We show that it interferes with αIIbβ3 activation, degranulation, and actin cytoskeleton remodeling, delaying thrombus formation in vivo — likely via modulation of AKT/VASP signaling.

These findings highlight a surprising dual role of apoC3 and underscore the complex interplay between lipid metabolism and thrombosis.