Inhaltspezifische Aktionen


Pathways for BMP9/10 responsiveness in smooth muscle cells, critical for pulmonary hypertension and right heart failure

BMP9 and BMP10 bind to the ALK1 receptor, which is linked to pulmonary hypertension (PH). We found that genetic inactivation of BMP9/10 in mice causes dramatic changes in vascular tone and diminution of vascular smooth muscle cells (VSMC), protecting mice from hypoxia-induced PH. These effects are mediated by vascular bed-specific expression of Alk receptors in VSMC. We will elucidate the impact of the BMP9/BMP10/Alk1 axis on reverse remodeling of pulmonary arteries, analyze the meaning of heterogeneous Alk-receptor expression in VSMCs, explore the cross-talk between Alk1/Smad1/5/8 and YAP-TEAD signaling and elucidate the impact of BMP9/10 dependent differential splicing in VSMCs.