Lysophosphatidylcholine (LPC) (LPC)

Lysophosphatidylcholine (LPC) is a class of bioactive signaling lipids produced primarily through the hydrolysis of phosphatidylcholine by phospholipase A2 (PLA2) enzymes or via the action of lecithin-cholesterol acyltransferase (LCAT) (Law et al., 2019). As a major phospholipid component of oxidized low-density lipoprotein (oxLDL), LPC plays a pivotal role in the pathogenesis of atherosclerosis by inducing endothelial dysfunction, promoting the expression of adhesion molecules, and stimulating the migration of monocytes and T-lymphocytes (Schmitz & Ruebsaamen, 2010). Beyond its pro-inflammatory roles, LPC serves as an endogenous ligand for several G protein-coupled receptors, most notably GPR119, which is involved in glucose-stimulated insulin secretion, and GPR132 (G2A), which modulates immune cell function (Soga et al., 2005; Kabarowski, 2009). Although LPC is a metabolite rather than a protein target, its levels are therapeutically relevant; for example, inhibitors of lipoprotein-associated phospholipase A2 (Lp-PLA2), such as darapladib, were developed to reduce vascular LPC concentrations and stabilize atherosclerotic plaques (Law et al., 2019). Furthermore, plasma LPC levels are utilized as clinical biomarkers, where decreased concentrations are often observed in states of systemic inflammation like sepsis or in certain malignancies, reflecting altered lipid metabolism (Drobnik et al., 2003).

Other names

LysoPCLysolecithin1-acyl-sn-glycero-3-phosphocholineL-alpha-Lysophosphatidylcholine

Inhibition of phospholipase A2 enzymes (e.g., Lp-PLA2, sPLA2) to reduce the production of LPC from phosphatidylcholine; binding to G protein-coupled receptors (GPR119, GPR132) to modulate downstream signaling (Law et al., 2019; Soga et al., 2005).