Pulmonary arterial hypertension (PAH) comprises a multifactorial group of pulmonary vascular disorders that cause pulmonary vascular remodeling and right heart failure. We previously found that Ophiocordyceps sinensis (OCS) suppressed the activity of TRPM7 channel, a key molecule accelerating the fibrotic process of cardiovascular remodeling. Thus, in this study, we explored the therapeutic potential of OCS for PAH and the mechanism involved therein.
In in vitro experiments, OCS suppressed a TRPM7 channel activity and TGF-β2-induced endothelial-to-mesenchymal transition (EndoMT) in human pulmonary arterial endothelial cells, and abnormally enhanced proliferation of pulmonary arterial smooth muscle cells from PAH patients. Moreover, in vivo experiments using PAH model rats and mice showed that OCS ameliorated the development of pulmonary artery thickening, cardiac fibrosis and right ventricle hypertrophy with normalization of heightened right ventricle pressure.  
These results suggest that OCS can ameliorate the pathology and cardiac dysfunction associated with pulmonary hypertension via TRPM7 inhibition. These findings could serve as an important clue to developing a new combinatorial PAH treatment.

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