ReviewFrontiers in cardiovascular medicine2022
Metabolic reprogramming: A novel metabolic model for pulmonary hypertension.
Review in Frontiers in cardiovascular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 14 citations in OpenAlex.
- The Role of Platelets in Pulmonary Hypertension: From Activation to Pulmonary Vascular Remodeling-A Review Article.Biomedicines · 2026Review
- Exploring the therapeutic potential of GLP-1 receptor agonists in pulmonary arterial hypertension.ERJ open research · 2026Review
- Paradigm shift: from pulmonary vasodilation to cardiopulmonary dual-track therapy-a comprehensive review of pathophysiology and advances in pulmonary hypertension-associated right heart failure.Respiratory research · 2026Review
- Roles of Lipid Metabolism in Pulmonary Hypertension: Friend or Foe?Biomolecules · 2025Review
- C-type natriuretic peptide attenuates enhanced glycolysis and de novo pyrimidine synthesis in pericytes of patients with pulmonary arterial hypertension.Communications biology · 2025Article
- The mitochondrial unfolded protein response and metabolic reprogramming promote PASMC proliferation in response to sphingosine kinase-1/sphingosine-1-phosphate signaling.bioRxiv : the preprint server for biology · 2025Article
- Restoration of pp60International journal of molecular sciences · 2025Article
- Oroxylin A, a broad‑spectrum anticancer agent, relieves monocrotaline‑induced pulmonary arterial hypertension by inhibiting the Warburg effect in rats.Molecular medicine reports · 2024Article
- Glycolysis Reprogramming in Idiopathic Pulmonary Fibrosis: Unveiling the Mystery of Lactate in the Lung.International journal of molecular sciences · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pulmonary arterial hypertension, or PAH, is a condition that is characterized by pulmonary artery pressures above 20 mmHg (at rest). In the treatment of PAH, the pulmonary vascular system is regulated to ensure a diastolic and contraction balance; nevertheless, this treatment does not prevent or reverse pulmonary vascular remodeling and still causes pulmonary hypertension to progress. According to Warburg, the link between metabolism and proliferation in PAH is similar to that of cancer, with a common aerobic glycolytic phenotype. By activating HIF, aerobic glycolysis is enhanced and cell proliferation is triggered. Aside from glutamine metabolism, the Randle cycle is also present in PAH. Enhanced glutamine metabolism replenishes carbon intermediates used by glycolysis and provides energy to over-proliferating and anti-apoptotic pulmonary vascular cells. By activating the Randle cycle, aerobic oxidation is enhanced, ATP is increased, and myocardial injury is reduced. PAH is predisposed by epigenetic dysregulation of DNA methylation, histone acetylation, and microRNA. This article discusses the abnormal metabolism of PAH and how metabolic therapy can be used to combat remodeling.
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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.