ReviewAmerican journal of physiology. Lung cellular and molecular physiology2020
The hallmarks of severe pulmonary arterial hypertension: the cancer hypothesis-ten years later.
Review in American journal of physiology. Lung cellular and molecular physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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.
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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
40 citing papers in PubMed, 60 citations in OpenAlex.
- Endothelial c-IAP2 loss amplifies P2X7 receptor-driven inflammation and worsens schistosomiasis-associated pulmonary hypertension.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Transcriptional landscape of pulmonary artery endothelium reveals subpopulation- and disease-specific remodeling signatures.Communications biology · 2026Article
- Emerging significance of E3 ubiquitin ligases and Deubiquitinases in pulmonary hypertension.Molecular medicine (Cambridge, Mass.) · 2026Review
- Article
- Liver bypass in the development of pathogen-associated pulmonary vascular disease: contribution of mesocaval and portosystemic shunts.American journal of physiology. Gastrointestinal and liver physiology · 2025Review
- SPP1 May Play an Important Role in the Carcinoid Nature of PAH.Mediators of inflammation · 2025Article
- Article
- Infection and pulmonary vascular diseases consortium: United against a global health challenge.Pulmonary circulation · 2024Article
- Current Overview of the Biology and Pharmacology in Sugen/Hypoxia-Induced Pulmonary Hypertension in Rats.Journal of aerosol medicine and pulmonary drug delivery · 2024Review
- PDZ-Binding Kinase, a Novel Regulator of Vascular Remodeling in Pulmonary Arterial Hypertension.Circulation · 2024Article
- Recent progress in the roles of microRNAs in pulmonary arterial hypertension associated with congenital heart disease.Narra J · 2024Review
- Autonomic nervous modulation: early treatment for pulmonary artery hypertension.ESC heart failure · 2024Review
- Emerging Trends in Pathophysiology: Insights from the 9th International Congress of the International Society for Pathophysiology (ISP 2023).Pathophysiology : the official journal of the International Society for Pathophysiology · 2024Article
- Host Transcriptional Regulatory Genes and Microbiome Networks Crosstalk through Immune Receptors Establishing Normal and Tumor Multiomics Metafirm of the Oral-Gut-Lung Axis.International journal of molecular sciences · 2023Review
- Purine synthesis suppression reduces the development and progression of pulmonary hypertension in rodent models.European heart journal · 2023Article
- Activation of PPAR-γ prevents TERT-mediated pulmonary vascular remodeling in MCT-induced pulmonary hypertension.Heliyon · 2023Article
- Tensions in Taxonomies: Current Understanding and Future Directions in the Pathobiologic Basis and Treatment of Group 1 and Group 3 Pulmonary Hypertension.Comprehensive Physiology · 2023Review
- Lung Cancer Gene Regulatory Network of Transcription Factors Related to the Hallmarks of Cancer.Current issues in molecular biology · 2023Article
- Schistosomiasis-associated pulmonary hypertension unveils disrupted murine gut-lung microbiome and reduced endoprotective Caveolin-1/BMPR2 expression.Frontiers in immunology · 2023Article
- Myeloid-derived suppressor cells and pulmonary hypertension.Frontiers in immunology · 2023Review
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Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
Abstract
Severe forms of pulmonary arterial hypertension (PAH) are most frequently the consequence of a lumen-obliterating angiopathy. One pathobiological model is that the initial pulmonary vascular endothelial cell injury and apoptosis is followed by the evolution of phenotypically altered, apoptosis-resistant, proliferating cells and an inflammatory vascular immune response. Although there may be a vasoconstrictive disease component, the increased pulmonary vascular shear stress in established PAH is caused largely by the vascular wall pathology. In this review, we revisit the "quasi-malignancy concept" of severe PAH and examine to what extent the hallmarks of PAH can be compared with the hallmarks of cancer. The cancer model of severe PAH, based on the growth of abnormal vascular and bone marrow-derived cells, may enable the emergence of novel cell-based PAH treatment strategies.
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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 OpenQuestion graph.