Ets2, also known as V-ets erythroblastosis virus E26 oncogene homolog 2, is a transcription factor belonging to the E26 transformation-specific sequence (ETS) domain family. It plays crucial roles in regulating cell proliferation, differentiation, apoptosis, and tumorigenesis, and is involved in multiple signaling pathways such as the MAPK/Erk and calcineurin/NFAT pathways [1,2].

In cardiac hypertrophy, conditional deletion of Ets2 in mouse cardiomyocytes protects against pressure-overload induced cardiac hypertrophy, and silencing Ets2 in the hearts of calcineurin transgenic mice attenuates hypertrophic growth and contractile dysfunction. Ets2 forms a complex with NFAT to stimulate transcriptional activity of hypertrophy-stimulated genes, revealing its role in the pathogenesis of cardiac hypertrophy [1].

In renal fibrosis, knockdown of Ets2 abrogates TGF-β1-mediated expression of profibrogenic factors in human proximal tubular epithelial cells, suggesting that Ets2 promotes epithelial-to-mesenchymal transition in renal fibrosis by targeting JUNB transcription [3].

In conclusion, Ets2 is a key transcription factor involved in multiple biological processes and disease conditions. Gene knockout and conditional knockout mouse models have significantly contributed to understanding its role in cardiac hypertrophy and renal fibrosis. These functional studies provide important insights into the underlying molecular mechanisms of related diseases, potentially paving the way for new therapeutic strategies.