CXCR2, a G-protein-coupled receptor, is one of the 20 chemokine receptors. Its well-known ligands include CXCL8 (IL-8) and CXCL1 (GRO-α). CXCR2 is crucial for the migration of immune system cells and tumor cells, as well as metastasis, by participating in chemokine-mediated signaling pathways [1]. It is involved in various biological processes such as cell proliferation, migration, and angiogenesis [1]. Gene knockout mouse models have been valuable in studying CXCR2 function.

In lung cancer, inhibition of CXCR2 in animal models promoted apoptosis, senescence, and anti-proliferation of lung cancer cells. Blocking CXCR2 also enhanced the therapeutic effect of cisplatin by regulating neutrophil infiltration, suggesting its importance in cancer treatment [2].

In hypertensive retinopathy, CXCR2 knockout mice showed ameliorated symptoms of arteriolar remodelling, macrophage infiltration, oxidative stress, and retinal dysfunction induced by angiotensin II, indicating the role of CXCR2 in this disease [3].

In angiotensin II-induced cardiac hypertrophy and remodelling, CXCR2 knockout mice and wild-type mice treated with a CXCR2 inhibitor had attenuated cardiac remodelling and inflammatory response, highlighting the role of CXCR2 in cardiac diseases [4].

In conclusion, CXCR2 plays essential roles in multiple biological processes, especially in cancer and various inflammatory-related diseases. Studies using CXCR2 knockout mouse models have significantly contributed to revealing its functions in specific disease conditions, providing potential therapeutic targets for treating lung cancer, hypertensive retinopathy, and cardiac diseases.