OXSR1, oxidative stress-responsive 1, is involved in multiple biological processes. It is associated with the WNK signalling pathway, which controls intracellular potassium balance [1]. In addition, it is implicated in various disease-related pathways, including those related to inflammation, cancer progression, and oxidative stress-related cellular responses. Genetic models, such as gene knockout (KO) or conditional knockout (CKO) mouse models, can be valuable for studying its function.

In mycobacterial infection, genetic depletion of OXSR1 decreases bacterial burden and intracellular potassium levels, and activates the NLRP3 inflammasome, caspase-mediated release of IL-1β, and downstream activation of protective TNF-α, suggesting its role in host-pathogen interaction [1]. In hepatocellular carcinoma (HCC), knockdown of LINC01291, which can up-regulate OXSR1 by sponging miR-186-5p, inhibits HCC cell proliferation, migration, invasion, and epithelial-mesenchymal progression (EMT), indicating that OXSR1 promotes HCC development [2]. Also, down-regulation of OXSR1 in HCC represses cell proliferation, migration, and invasion both in vivo and in vitro [4]. In septic myocardial injury, silencing circROCK1, which is related to OXSR1 through the miR-96-5p axis, improves cardiac function and reduces myocardial injury [3].

In conclusion, OXSR1 plays essential roles in biological processes like host-pathogen interaction and cancer development. Studies using KO/CKO mouse models related to OXSR1 have contributed to understanding its functions in mycobacterial infection and HCC. These findings suggest that targeting OXSR1 could potentially be a strategy for treating intracellular infections and HCC.