Phospholipase A2 group V (PLA2G5)

Phospholipase A2 group V (PLA2G5) is a secreted, calcium-dependent enzyme that hydrolyzes the sn-2 position of membrane phospholipids, generating free fatty acids (including arachidonic acid) and lysophospholipids[1][4][6]. It is widely expressed in innate immune cells (such as neutrophils and macrophages), vascular tissue, the retina, and the liver. PLA2G5 plays a critical role in promoting inflammatory signaling, modulating lipid mediator synthesis, modifying LDL in atherogenesis, regulating vascular permeability, and influencing antiviral defense in the lung. Genetic alterations in PLA2G5 can cause benign familial fleck retina, while its expression and activity have been linked to cardiovascular disease, inflammation, and some cancers where its gene may be epigenetically silenced[1][4][6]. Selective inhibition of secretory PLA2s, including PLA2G5, has been explored therapeutically for inflammatory and cardiovascular diseases, though no approved selective inhibitors are currently available for this isoform[1][7].

Other names

Phospholipase A2 group VPLA2G5PLA2-10Phosphatidylcholine 2-acylhydrolase 5FRFBGV-PLA2hVPLA(2)Ca2+-dependent phospholipase A2calcium-dependent phospholipase A2

Secretory PLA2 (Ca2+-dependent) inhibition blocks hydrolysis of phospholipids, thereby reducing proinflammatory lipid mediators and downstream eicosanoid signaling.