Bone morphogenetic proteins (BMPs) were originally identified as inducers of ectopic bone growth and cartilage formation, whereas emerging literature reported the multiple functions of these growth factors, including regulating cell growth, differentiation, and apoptosis of various cell types. In particular, BMP-9 is expressed in the adult liver by nonparenchymal cells as well as in the septum and spinal cord of mouse embryos2. Duan et al. (2024) recently reported the potential protective effects of BMP-9 against myocardial infarction (MI). Based on expressional profiles of BMP-9 in cardiac tissues and plasma samples, circulating BMP-9 and its cardiac levels are markedly increased in humans and mice with MI and are negatively associated with cardiac function. While BMP-9 deficiency exacerbates MI-related changes in mice models, replenishment of BMP-9 significantly attenuates these adverse effects. The research team further demonstrated that BMP-9 improved lymphatic drainage function and hence reduced cardiac oedema. Interestingly, the results also indicated that BMP-9 increased the expression of mitochondrial DECR1 (2,4-dienoyl-CoA reductase 1) which promotes cardiac mitochondrial bioenergetics and mitigates MI-induced cardiomyocyte injury3. Therefore, it is likely that BMP-9 protects against MI by improving lymphatic drainage function and triggering DECR1-mediated mitochondrial bioenergetics.
References
2. David et al. Circ Res 2008; 102: 914–22. 3. Duan et al. Circulation 2024. DOI:10.1161/CIRCULATIONAHA.123.065935.
