Bmp6, or Bone Morphogenetic Protein 6, is part of the transforming growth factor-beta (TGF-β) superfamily. It is involved in multiple biological functions such as iron homeostasis, cell-cell interactions, angiogenesis, and the regulation of stem cell self-renewal and differentiation [2,4]. The BMP6/SMADs signaling pathway is one of its associated pathways, which has implications in inflammation, ferroptosis, and cell polarization [1].

In a mouse myocardial infarction model, BMP6 -/- mice showed more significant decline in cardiac function, enlarged infarct area, increased fibrosis, and more pronounced inflammatory infiltration compared to wild-type mice. Knocking down BMP6 promoted AP-1 phosphorylation, accelerating cardiac fibrosis progression, indicating that BMP6 may be a target for improving myocardial fibrosis and cardiac function after myocardial infarction [3]. In a melanoma mouse model, BMP6 deficiency caused significantly delayed tumor onset and decelerated tumor progression, suggesting its role in tumor micro-environment modulation [5]. In zebrafish embryos, knockout of BMP6 significantly increased the deformity rate, suggesting its role in regulating the abnormal osteogenic differentiation of bone-marrow-derived mesenchymal stem cells in adolescent idiopathic scoliosis [6].

In conclusion, Bmp6 plays essential roles in various biological processes including cardiac repair, tumor development, and bone metabolism. Gene knockout models in mice and zebrafish have revealed its significance in specific disease areas such as myocardial infarction, melanoma, and adolescent idiopathic scoliosis, providing potential molecular targets for treatment.