ReviewFrontiers in medicine2018
Pulmonary Arterial Stiffness: An Early and Pervasive Driver of Pulmonary Arterial Hypertension.
Review in Frontiers in medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
33 citing papers in PubMed.
- Beyond the Heart-Lung Axis: A Review of the Crosstalk Between the Hemodynamic, Neurohormonal, and Immune Systems in Pulmonary Hypertension.Comprehensive physiology · 2026Review
- Mesenchymal stromal cells alleviate pulmonary arterial hypertension by suppressing pulmonary arterial adventitial fibroblast activation and extracellular matrix remodeling via the SOCS3/STAT3 pathway.Stem cell research & therapy · 2026Article
- Female Fibroblast Activation Is Estrogen-Mediated in Sex-Specific 3D-Bioprinted Pulmonary Artery Adventitia Models.ACS biomaterials science & engineering · 2025Article
- Vascular Remodeling: The Multicellular Mechanisms of Pulmonary Hypertension.International journal of molecular sciences · 2025Review
- Differences in Pulmonary Artery Stiffness Measured by CMR in Preterm-Born Young Adults With and Without Bronchopulmonary Dysplasia.Circulation. Cardiovascular imaging · 2025Article
- Impact of Laparoscopic Sleeve Gastrectomy on Pulmonary Arterial Stiffness and Right Ventricular Function in Obese Patients.Obesity surgery · 2025Article
- Transition from parenteral treprostinil to selexipag aiming at hemodynamic targets in pulmonary arterial hypertension.Clinical hypertension · 2025Article
- YAP/TAZ as mechanobiological signaling pathway in cardiovascular physiological regulation and pathogenesis.Mechanobiology in medicine · 2024Article
- Selenium supplementation elevated SELENBP1 to inhibit fibroblast activation in pulmonary arterial hypertension.iScience · 2024Article
- Pulmonary Hypertension Induced by Right Pulmonary Artery Occlusion: Hemodynamic Consequences ofJournal of the American Heart Association · 2024Article
- Dynamically stiffening biomaterials reveal age- and sex-specific differences in pulmonary arterial adventitial fibroblast activation.Matrix biology plus · 2024Article
- Multi-scaled temporal modeling of cardiovascular disease progression: An illustration of proximal arteries in pulmonary hypertension.Journal of biomechanics · 2024Article
- Pathophysiology and pathogenic mechanisms of pulmonary hypertension: role of membrane receptors, ion channels, and CaPhysiological reviews · 2023Review
- Functional and molecular determinants of right ventricular response to severe pulmonary hypertension in a large animal model.American journal of physiology. Heart and circulatory physiology · 2023Article
- Uncertainty Quantification in the In Vivo Image-Based Estimation of Local Elastic Properties of Vascular Walls.Journal of cardiovascular development and disease · 2023Article
- Role of macrophages in pulmonary arterial hypertension.Frontiers in immunology · 2023Review
- 3D-bioprinted, phototunable hydrogel models for studying adventitial fibroblast activation in pulmonary arterial hypertension.Biofabrication · 2022Article
- Cross-talk between TSC2 and the extracellular matrix controls pulmonary vascular proliferation and pulmonary hypertension.Science signaling · 2022Article
- Hemodynamically Unloading the Distal Pulmonary Circulation in Pulmonary Hypertension: A Modeling Study.Journal of biomechanical engineering · 2022Article
- The Role of Glutamine and Glutaminase in Pulmonary Hypertension.Frontiers in cardiovascular medicine · 2022Review
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Pulmonary arterial hypertension (PAH) is a historically neglected and highly morbid vascular disease that leads to right heart failure and, in some cases, death. The molecular origins of this disease have been poorly defined, and as such, current pulmonary vasodilator therapies do not cure or reverse this disease. Although extracellular matrix (ECM) remodeling and pulmonary arterial stiffening have long been associated with end-stage PAH, recent studies have reported that such vascular stiffening can occur early in pathogenesis. Furthermore, there is emerging evidence that ECM stiffening may represent a key first step in pathogenic reprogramming and molecular crosstalk among endothelial, smooth muscle, and fibroblast cells in the remodeled pulmonary vessel. Such processes represent the convergence of activation of a number of specific mechanoactivated signaling pathways, microRNAs, and metabolic pathways in pulmonary vasculature. In this review, we summarize the contemporary understanding of vascular stiffening as a driver of PAH, its mechanisms, potential therapeutic targets and clinical perspectives. Of note, early intervention targeting arterial stiffness may break the vicious cycle of PAH progression, leading to outcome improvement which has not been demonstrated by current vasodilator therapy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.