Key result
BMPR2 mutation is linked to worse RV function than noncarrier status despite similar afterload.
Why the study?
Right ventricular function is more severely affected in pulmonary arterial hypertension patients with BMPR2 mutation than in noncarriers, but the underlying mechanisms are unclear.
Does Bone Morphogenetic Protein Receptor Type 2 (BMPR2) mutation affect RV function and signaling pathways in patients with pulmonary arterial hypertension?
Does Bone Morphogenetic Protein Receptor Type 2 (BMPR2) mutation affect RV function and signaling pathways in patients with pulmonary arterial hypertension?
BMPR2 mutation carriers with PAH have worse RV function than noncarriers, which is not explained by differences in TGF-β or BMPR2 signaling.
Supports closer RV monitoring in BMPR2-mutation PAH; leaves open alternative pathways and prospective validation.
Despite a similar afterload, RV function is more severely affected in mutation carriers than in noncarriers. However, these differences cannot be explained by a differential transforming growth factor β, bone morphogenetic protein receptor II signaling, or cardiac adaptation.
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Bruggen et al. (2016) studied this question. Bone morphogenetic protein receptor type 2 mutation carriers exhibit more severely impaired right ventricular function than noncarriers despite similar afterload.
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