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Abstract
In pulmonary hypertension (PH), therapies targeting various pathways may improve clinical status but often leave established vascular remodelling incompletely reversible.
- Increased right ventricular afterload and persistent pulmonary vascular remodelling are key features of PH.
- Vascular ageing may influence the residual remodelling load in PH, particularly through stress-induced cell changes.
- Endothelial repair failure and extracellular matrix stiffening are processes that reduce vascular flexibility and contribute to disease progression.
- Pharmacological strategies being explored include treatments that target cellular senescence and modulate specific growth factors.
- Future studies on PH are suggested to focus on endpoints that connect molecular targets to pulmonary vascular function and safety.
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