Pla2g2a, encoding secreted group IIA-phospholipase A2 (sPLA2-IIA), hydrolyzes glycerophospholipids at the sn-2 position, releasing fatty acids and lysophospholipids. It is involved in multiple biological processes such as anti-bacterial defense, inflammation, eicosanoid generation, and clearance of apoptotic cells, and is associated with pathways like MAPK/Erk, NF-κB, and Wnt signaling [2,5]. Genetic models like KO mouse models are valuable for studying its functions.

In pancreatic cancer, PLA2G2A+ cancer-associated fibroblasts impede the antitumor immune response of CD8+ cytotoxic T cells, facilitating tumor immune escape via MAPK/Erk and NF-κB signaling pathways, and are related to poor prognosis [1].

In the context of innate immunity, loss of Pla2g2a in BALB/c mice background decreased IL-5 from Th2-type ILC2s and NKT2s, increased bacterial-reactive NKT17 cells and MAIT cells, and decreased early-generated B1a cells [2].

In idiopathic pulmonary fibrosis, PLA2G2A is significantly correlated with poor patient prognosis and can predict mortality rates [3].

In pancreatic cancer cells with K-ras mutation, PLA2G2A promotes fatty acid synthesis and energy metabolism, and its inhibition increases lipid peroxidation and impairs mitochondrial function [4].

In carotid atherosclerosis, high expression of PLA2G2A in fibroblasts promotes plaque progression through macrophage complement and coagulation cascade pathways in the early-stage [6].

In conclusion, Pla2g2a plays diverse and crucial roles in various biological processes and disease conditions. Studies using KO mouse models and other loss-of-function experiments have revealed its significant impact on cancer immune escape, innate immunity, fibrosis, lipid metabolism, and atherosclerosis. These findings provide valuable insights into understanding disease mechanisms and potential therapeutic targets related to Pla2g2a.