Ets1, also known as E26 oncogene homolog 1, is a transcription factor. It is critically involved in various biological processes such as cell development, differentiation, proliferation, apoptosis, migration, and tissue remodeling. Ets1 belongs to the Ets family of transcription factors, and its DNA-binding activity is regulated by kinases and other transcription factors. It is associated with multiple pathways and is of great biological importance in normal cell function and disease development [2,4,5].

In a hyperoxia-induced bronchopulmonary dysplasia (BPD) mouse model, Ets1 overexpression increased cell viability, glucose consumption, lactate production, and NADPH levels in A549 cells and reduced inflammation and apoptosis. In BPD mice, it prevented weight loss, airway enlargement, and alveolar count reduction. Ets1 binds to the Nrf2 promoter region, promoting Nrf2 transcription, and its overexpression increased the levels of Nrf2-related proteins. This indicates that Ets1 is important in oxidative stress-related ferroptosis in BPD, partially mediated by the Nrf2/HO-1 axis [1]. In Ets1 knockout mice, a lupus-like autoimmune disease develops, with enhanced activation and differentiation of both B cells and T cells, suggesting Ets1's role in autoimmune disease regulation [3].

In conclusion, Ets1 plays a crucial role in multiple biological processes and diseases. Its functions in BPD, as revealed by mouse models, are related to oxidative stress-associated ferroptosis regulation. In autoimmune diseases, Ets1 knockout mouse models show its importance in maintaining immune cell homeostasis. Understanding Ets1's functions through these models provides insights into disease mechanisms and potential therapeutic targets.