Key result
Pulmonary arterial smooth muscle cells dynamically modulate their phenotype, contributing to the onset and progression of pulmonary arterial hypertension.
Why the study?
The dysfunction and molecular mechanisms underlying pulmonary arterial smooth muscle cell phenotypic diversity and contribution to pulmonary vascular lesions in PAH remain a major focus of research.
This review highlights the phenotypic diversity and origins of vascular smooth muscle cells in pulmonary arterial hypertension, identifying potential molecular targets for future therapies.
May inform PAH therapies targeting smooth muscle phenotype modulation; leaves open clinical validation in prospective studies.
Pulmonary arterial hypertension (PAH) is a progressive incurable condition that is characterized by extensive remodeling of the pulmonary circulation, leading to severe right-sided heart failure and death. Similar to other vascular contractile cells, pulmonary arterial smooth muscle cells play central roles in physiological and pathologic vascular remodeling because of their remarkable ability to dynamically modulate their phenotype to ensure contractile and synthetic functions. The dysfunction and molecular mechanisms underlying their contribution to the various pulmonary vascular lesions associated with PAH have been a major focus of research. The aim of this review is to describe the medial and nonmedial origins of contractile cells in the pulmonary vascular wall and present evidence of how they contribute to the onset and progression of PAH. We also highlight specific potential target molecules and discuss future directions that are being explored to widen the therapeutic options for the treatment of PAH.
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Lechartier et al. (2021) conducted a review in Pulmonary arterial hypertension. Pulmonary arterial smooth muscle cells dynamically modulate their phenotype, contributing to the onset and progression of pulmonary arterial hypertension.
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