ArticlePulmonary circulation2012
New models of pulmonary hypertension based on VEGF receptor blockade-induced endothelial cell apoptosis.
Article in Pulmonary circulation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
69 citing papers in PubMed, 1 synthesis or guideline pooled it, 107 citations in OpenAlex.
- Prognostic significance of pulmonary hypertension in patients with cystic fibrosis: A systematic review and meta-analysis.Medicine · 2018Pooled it
- Hypoxia Induces Adaptive Lymphangiogenesis via Cd74 and Vegfr3 to Modulate Pulmonary Hypertension.Circulation research · 2026Article
- Right Ventricular Free Wall Strain in Healthy Lowlanders and Highlanders-A Case-Control Study.Journal of clinical medicine · 2026Article
- Deciphering the Counterintuitive Role of Vascular Endothelial Growth Factor Signaling Pathways in Pulmonary Arterial Hypertension.International journal of molecular sciences · 2026Review
- Fenofibrate as a Modulator of the Renin-Angiotensin System in Su/Hx-Induced Pulmonary Arterial Hypertension.International journal of molecular sciences · 2025Article
- Echocardiographic Assessment of Pulmonary Hemodynamics and Right Ventricular Performance in Neonatal Murine Hypoxia.Journal of cardiovascular development and disease · 2025Article
- The vascular phenotype of BPD: new basic science insights-new precision medicine approaches.Pediatric research · 2024Review
- Converging Pathways: A Review of Pulmonary Hypertension in Interstitial Lung Disease.Life (Basel, Switzerland) · 2024Review
- Pneumonectomy combined with SU5416 or monocrotaline pyrrole does not cause severe pulmonary hypertension in mice.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Endothelial Function in Pulmonary Arterial Hypertension: From Bench to Bedside.Journal of clinical medicine · 2024Review
- Reversal of Pulmonary Hypertension in a Human-Like Model: Therapeutic Targeting of Endothelial DHFR.Circulation research · 2024Article
- Unraveling the role of HIF and epigenetic regulation in pulmonary arterial hypertension: implications for clinical research and its therapeutic approach.Frontiers in medicine · 2024Review
- The biased apelin receptor agonist, MM07, reverses Sugen/hypoxia-induced pulmonary arterial hypertension as effectively as the endothelin antagonist macitentan.Frontiers in pharmacology · 2024Article
- IL-1β-mediated adaptive reprogramming of endogenous human cardiac fibroblasts to cells with immune features during fibrotic remodeling.Communications biology · 2023Article
- An emerging class of new therapeutics targeting TGF, Activin, and BMP ligands in pulmonary arterial hypertension.Developmental dynamics : an official publication of the American Association of Anatomists · 2023Review
- Inflammation and immunity in the pathogenesis of hypoxic pulmonary hypertension.Frontiers in immunology · 2023Review
- Cytokine profiling in pulmonary arterial hypertension: the role of redox homeostasis and sex.Translational research : the journal of laboratory and clinical medicine · 2022Article
- Pulmonary Arterial Hypertension and Consecutive Right Heart Failure Lead to Liver Fibrosis.Frontiers in cardiovascular medicine · 2022Article
- The inflammatory role of dysregulated IRS2 in pulmonary vascular remodeling under hypoxic conditions.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- Response to Michiel Alexander de Raaf et al.Hypertension research : official journal of the Japanese Society of Hypertension · 2021Article
9 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 5 institutions in 3 countries.
Funding
Abstract
In spite of treatment, severe angioproliferative pulmonary arterial hypertension (PAH) remains a disease characterized by great morbidity and shortened survival. New treatment strategies for patients with PAH are needed, and after drug development, preclinical studies are best conducted in animal models which present with pulmonary angio-obliterative disease and right heart failure. A rat model of severe pulmonary hypertension and right heart failure, described a decade ago, continues to be investigated and provide insight into the nature of the lung vascular lesions and mechanisms of cardiac adaptation to an altered lung circulation. This rat model is based on the combination of VEGF receptor blockade with Su5416 and chronic hypoxia; use of this pulmonary hypertension induction strategy led to developing the concept of apoptosis-dependent compensatory vascular cell growth. Although, often employed in experimental designs, chronic hypoxia is not necessary for the development of angio-obliterative pulmonary hypertension. Left pneumonectomy combined with Su5416 also results in severe pulmonary hypertension in normoxic conditions. Similarly, the immune insufficiency component of severe PAH can be modeled in athymic rats (lacking T-lymphocytes). In these rats housed under normoxic conditions, treatment with the VEGFR receptor blocker results in angioproliferative pulmonary hypertension; cardiopulmonary disease in these animals can be prevented by immune reconstitution of regulatory T-cells (Tregs). Finally, chronic hypoxia can be replaced with another stimulator of HIF-1α: Ovalbumin (Ova). Immunization of rats with Ova increases lung tissue HIF-1α protein expression, and in Su5416-treated rats causes lethal pulmonary hypertension. Finally, we postulate that these models may also be useful for "reverse translation"; that is, the mechanisms of lung vascular cell death and growth and the modifying influences of immune and bone marrow cells that have been identified in the Su5416 VEGFR inhibitor models can be informative about heretofore undescribed processes in human PAH.
Indexed as
Identifiers
What OpenQuestion holds
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.