
-   In murine models, Anxa2 mRNA expression in the renal cortex is significantly elevated on day 3 after acute tubular necrosis induced by uranyl nitrate. This elevation in Anxa2 expression occurs alongside S100A6 upregulation and is confirmed during the proliferative recovery phase of acute renal failure, associated with cell proliferation markers like PCNA and dedifferentiation markers such as vimentin. Similar upregulation of Anxa2 is observed in other kidney injury models like ischemia-reperfusion injury and folic acid-induced acute renal failure [PMID: 16316344].
-   ANXA2 expression in clear cell renal cell carcinoma (ccRCC) is functionally associated with the Hippo signaling pathway. Specifically, ANXA2 interacts with DBT, leading to the activation of Hippo signaling, resulting in transcriptional repression of lipogenic genes, which hampers tumor progression and lipid accumulation in ccRCC. In the subcutaneous tumor mouse models, DBT overexpression yielded effective inhibition of tumor growth, while the knockdown of ANXA2 could reverse the growth inhibition, suggesting that the DBT-ANXA2-YAP axis suppressed tumor progression and inhibited lipid accumulation in ccRCC [PMID: 36860124].
-   In cisplatin-induced acute kidney injury (AKI) mouse models, the mRNA and protein expression of Annexin A2 (ANXA2) increased in renal tubules. Ectopic expression of ANXA2 improved lysosomal function and autophagic flux, thereby reducing renal tubular cell apoptosis and mitigating kidney injury. The beta-catenin signaling pathway was identified as key in this process, with ANXA2 enhancing beta-catenin activation, which subsequently upregulated transcription factor EB (TFEB), leading to increased lysosome biogenesis and improved autophagy [PMID: 36307397].
