Bmi1, also known as B-cell-specific Moloney murine leukemia virus integration site-1, is a member of the PRC1 family and a well-recognized transcriptional suppressor. It has the ability to maintain the self-renewal and proliferation of tissue-specific stem cells. Bmi1 is involved in various cellular processes such as cell cycle progression, senescence, apoptosis, and angiogenesis. It functions through pathways like the INK4a/ARF locus, NF-κB signaling pathway, and PTEN/PI3K/AKT signaling pathway [1,2,3,5].

In the heart, emerging data show that Bmi1 is expressed in heart tissue and impacts various cardiac pathological conditions. In multiple myeloma, BMI1-KO MM-Φs from BM cells of BMI1-KO mice exhibited reduced proliferation and suppressed expression of angiogenic factors, losing their pro-myeloma effects, indicating that BMI1 mediates the pro-myeloma functions of MM-MΦs [1,4]. In spermatogonial stem cells (SSCs), BMI1-deficient SSCs showed transcriptional activation of Wnt10b and nuclear translocation of β-catenin, and suppressing Wnt/β-catenin signaling restored SSC maintenance, revealing a mechanism for BMI1 in SSC maintenance [6].

In conclusion, Bmi1 is essential for maintaining the self-renewal and proliferation of tissue-specific stem cells. Studies using KO mouse models have revealed its roles in cardiac pathological conditions, multiple myeloma, and SSC maintenance. These findings provide insights into its functions in different biological processes and potential therapeutic implications for related diseases.