Saa2 is one of the members of the Serum Amyloid A (SAA) protein family. SAA proteins are small, well-conserved in mammalian evolution, and are prominently synthesized in the liver. Saa2, along with SAA1, are key players in the acute phase response. They are lipophilic and contribute to high-density lipoproteins and cholesterol transport. Saa2 is also involved in various biological processes such as tissue remodeling, immune regulation, and has potential implications in host defense [1].

In a mouse model of intrauterine inflammation, placental Saa2 increased significantly. Maternal inhibition of Saa2 using siSaa2 markedly decreased preterm birth and downregulated the increased placental expression of pro-inflammatory cytokines Il1β, Il6, and Tnfα [3]. In the context of Th17-mediated inflammatory diseases, loss-and gain-of-function mouse models showed that Saa2, along with SAA1 and SAA3, have distinct systemic and local functions in promoting such diseases [2]. In inflammatory bowel disease, the expression of mesentery-derived Saa2 is upregulated, contributing to macrophage immunoregulation [4].

In conclusion, Saa2 is involved in multiple biological processes, especially in inflammation-related responses. Gene-knockout or loss-of-function mouse models have revealed its role in preterm birth, Th17-mediated inflammatory diseases, and inflammatory bowel disease, highlighting its potential as a therapeutic target in these disease areas.