BACH1, also known as BTB and CNC homology 1, is a transcription factor that regulates multiple physiological processes. It is involved in heme homeostasis, oxidative stress response, and is associated with pathways like glycolysis, angiogenesis, and insulin signaling. Genetic models, such as knockout (KO) mouse models, are valuable for studying its functions [1,2,3,4,5].

In endothelial cell-specific Bach1 knockout mice, deletion of BACH1 attenuated atherosclerosis by reducing endothelial inflammation, as it decreased atherosclerotic lesions, macrophage content, and adhesion molecule expression [1]. Hepatocyte-specific Bach1 deletion in male mice on a high-fat diet ameliorated hyperglycemia, insulin resistance, and steatosis, indicating its role in hepatic insulin signaling and glucose homeostasis [2]. Cardiac-specific BACH1 knockout in mice protected against angiotensin II-and transverse aortic constriction-induced cardiac hypertrophy and fibrosis, and preserved cardiac function, while overexpression exaggerated these phenotypes [5].

In conclusion, BACH1 is a key regulator in multiple biological processes. The use of KO mouse models has revealed its importance in diseases such as atherosclerosis, hepatic insulin-related disorders, and cardiac hypertrophy, providing insights into potential therapeutic targets for these conditions.

References:

1. Jia, Mengping, Li, Qinhan, Guo, Jieyu, Yu, Bo, Meng, Dan. 2022. Deletion of BACH1 Attenuates Atherosclerosis by Reducing Endothelial Inflammation. In Circulation research, 130, 1038-1055. doi:10.1161/CIRCRESAHA.121.319540. https://pubmed.ncbi.nlm.nih.gov/35196865/

2. Jin, Jiayu, He, Yunquan, Guo, Jieyu, Zhi, Xiuling, Meng, Dan. 2023. BACH1 controls hepatic insulin signaling and glucose homeostasis in mice. In Nature communications, 14, 8428. doi:10.1038/s41467-023-44088-z. https://pubmed.ncbi.nlm.nih.gov/38129407/

3. Padilla, Joselyn, Lee, Jiyoung. 2021. A Novel Therapeutic Target, BACH1, Regulates Cancer Metabolism. In Cells, 10, . doi:10.3390/cells10030634. https://pubmed.ncbi.nlm.nih.gov/33809182/

4. Wei, Xiangxiang, Guo, Jieyu, Li, Qinhan, Zhang, Shuning, Meng, Dan. 2019. Bach1 regulates self-renewal and impedes mesendodermal differentiation of human embryonic stem cells. In Science advances, 5, eaau7887. doi:10.1126/sciadv.aau7887. https://pubmed.ncbi.nlm.nih.gov/30891497/

5. Wei, Xiangxiang, Jin, Jiayu, Wu, Jian, Zhang, Jianyi, Meng, Dan. . Cardiac-specific BACH1 ablation attenuates pathological cardiac hypertrophy by inhibiting the Ang II type 1 receptor expression and the Ca2+/CaMKII pathway. In Cardiovascular research, 119, 1842-1855. doi:10.1093/cvr/cvad086. https://pubmed.ncbi.nlm.nih.gov/37279500/