Bone Morphogenetic Protein 9 Protects Against Myocardial Infarction by Improving Lymphatic Drainage Function and Triggering DECR1-Mediated Mitochondrial Bioenergetics
Authors' conclusion
These results suggest that BMP9 protects against MI by fine-tuning the multiorgan cross-talk among the liver, lymph, and the heart.
Study context
- Population
- Humans and mice with myocardial infarction (MI)
- Comparison
- BMP9 deficiency vs BMP9 replenishment in mice with MI
Main finding
As reported in the abstract
- Circulating and cardiac BMP9 markedly increased in humans and mice with MI, negatively associated with cardiac function
- BMP9 deficiency exacerbates LV dysfunction, increases infarct size and augments cardiac fibrosis in mice with MI; BMP9 replenishment significantly attenuates these effects
- BMP9 improves lymphatic drainage function, decreasing cardiac edema
- BMP9 increases mitochondrial DECR1 expression, promoting cardiac mitochondrial bioenergetics and mitigating MI-induced cardiomyocyte injury
- DECR1 deficiency exacerbates MI-induced cardiac damage in mice, restored by AAV-mediated DECR1; DECR1 deletion abrogates the benefit of BMP9
Original publication
Bone Morphogenetic Protein 9 Protects Against Myocardial Infarction by Improving Lymphatic Drainage Function and Triggering DECR1-Mediated Mitochondrial Bioenergetics. Circulation. Published 24 September 2024. doi:10.
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