Anxa1, also known as Annexin-A1, is a protein-coding gene. It is involved in multiple biological processes such as immune regulation, cell phenotype switching, and cholesterol transport [1,2,3]. In the immune system, it can regulate microglial activation. It also plays a role in pathways like the NF-κB pathway [1].

In an acute aortic dissection (AAD) murine model, systemic deficiency of Anxa1 markedly progressed AAD, indicating its role in preventing AAD by inhibiting vascular smooth muscle cell (VSMC) phenotype switching. Anxa1 deficiency in VSMCs triggered the synthetic phenotype via down-regulation of the JunB/MYL9 pathway, leading to elevated inflammation and enhanced matrix metalloproteinases production [2]. In microglia, administration of Tat-NTS peptide led to a shift of Anxa1 subcellular localization, an increase in Anxa1 SUMOylation, and a transformation of microglia towards an anti-inflammatory phenotype, reducing the activation of the NF-κB pathway and subsequent release of pro-inflammatory factors, thus protecting neurons against cerebral ischemia-reperfusion injury [1].

In conclusion, Anxa1 is crucial in immune regulation, especially in microglial activation related to cerebral ischemia-reperfusion injury, and in preventing AAD through its effect on VSMC phenotype switching. Gene knockout or conditional knockout mouse models have been instrumental in revealing these functions, providing potential therapeutic targets for these disease areas.