What this means
This review gathers earlier data on how aged, worn-out cells in lung blood vessels may slow recovery in pulmonary hypertension. It does not show that treating these cells helps patients.
Plain-English summary written by an AI model from the abstract. The original is below.
- Who it was tested in
- A review of earlier studies, not a new experiment
- Kind of research
- A summary of earlier studies
The science
- Original title
- Cellular Senescence and Vascular Ageing in Pulmonary Hypertension: Molecular Mechanisms, Therapeutic Strategies, and Translational Endpoints.
- Authors
- Chen Y, Wang X, Gao M et al.
- Journal
- Pulmonary pharmacology & therapeutics
- Published
- Oct 23, 2026
- Study type
- Review
- PMID
- 42918485 ↗
Abstract
Increased right ventricular afterload, persistent pulmonary vascular remodelling, and the development of right heart failure are the hallmarks of pulmonary hypertension (PH). In PAH, therapies targeting the prostacyclin, nitric oxide-cyclic guanosine monophosphate, and endothelin pathways improve clinical status and haemodynamics, although established vascular remodelling frequently remains incompletely reversible. This review summarises data suggesting that the residual remodelling load in PH is influenced by vascular ageing, specifically stress-induced premature senescence-like phenotypes in pulmonary vascular wall cells. Endothelial repair failure, pulmonary artery smooth muscle cell secretory amplification, extracellular matrix (ECM) stiffening, senescence-associated secretory phenotype signalling, and mechano-metabolic reprogramming are examined as interconnected processes that attenuate vascular plasticity and consolidate disease progression. Pharmacological strategies discussed include senolytic and senomorphic approaches, activin/TGF-β superfamily modulation exemplified by sotatercept, matrix- and mechanotransduction-directed interventions, and metabolic modulation. Finally, vascular ageing-informed PH studies are proposed to incorporate concordant endpoints that align molecular target engagement with pulmonary vascular mechanics, right ventricular-pulmonary arterial (RV-PA) coupling, right ventricular function, and safety outcomes.
Chen Y, Wang X, Gao M et al. Cellular Senescence and Vascular Ageing in Pulmonary Hypertension: Molecular Mechanisms, Therapeutic Strategies, and Translational Endpoints. Pulmonary pharmacology & therapeutics. 2026. doi:10.1016/j.pupt.2026.102454. PMID: 42918485. https://pubmed.ncbi.nlm.nih.gov/42918485/
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