ReviewFrontiers in cardiovascular medicine2021
Glutaminolysis: A Driver of Vascular and Cardiac Remodeling in Pulmonary Arterial Hypertension.
Review in Frontiers in cardiovascular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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Who cites it
14 citing papers in PubMed, 16 citations in OpenAlex.
- Alterations of endothelial cell bioenergetics in congenital diaphragmatic hernia.Pediatric research · 2026Article
- Beyond the Vasculature: The Emerging Role of Systemic Metabolism and Immunometabolism in Pulmonary Arterial Hypertension.International journal of molecular sciences · 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
- c-Myc promotes metabolic reprogramming in pulmonary hypertension via the stimulation of glutaminolysis and the reductive tricarboxylic acid cycle.Redox biology · 2025Article
- C-type natriuretic peptide attenuates enhanced glycolysis and de novo pyrimidine synthesis in pericytes of patients with pulmonary arterial hypertension.Communications biology · 2025Article
- Metabolic Alterations Associated With Right Ventricular Dysfunction in Pulmonary Arterial Hypertension: The Modulatory Effects and Improvement Mechanisms of Exercise.Reviews in cardiovascular medicine · 2025Review
- A multimodal approach identifies lactate as a central feature of right ventricular failure that is detectable in human plasma.Frontiers in medicine · 2024Article
- Targeting Mitochondrial Metabolic Dysfunction in Pulmonary Hypertension: Toward New Therapeutic Approaches?International journal of molecular sciences · 2023Review
- Mitochondrial Dysfunction in Pulmonary Hypertension.Antioxidants (Basel, Switzerland) · 2023Review
- Important Functions and Molecular Mechanisms of Mitochondrial Redox Signaling in Pulmonary Hypertension.Antioxidants (Basel, Switzerland) · 2022Review
- Mitochondrial Metabolism, Redox, and Calcium Homeostasis in Pulmonary Arterial Hypertension.Biomedicines · 2022Review
- Mechanism of tonifying-kidney Chinese herbal medicine in the treatment of chronic heart failure.Frontiers in cardiovascular medicine · 2022Review
- Metabolic reprogramming: A novel metabolic model for pulmonary hypertension.Frontiers in cardiovascular medicine · 2022Review
- Identification of novel metabolic signatures potentially involved in the pathogenesis of COPD associated pulmonary hypertension.Metabolomics : Official journal of the Metabolomic Society · 2021Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pulmonary arterial hypertension (PAH) is a decimating ailment described by chronic precapillary pulmonary hypertension, an elevated mean pulmonary arterial pressure with a normal pulmonary capillary wedge pressure, and a raised pulmonary vascular resistance resulting in increased right ventricular afterload culminating in heart failure and death. Current PAH treatments regulate the vasodilatory/vasoconstrictory balance of pulmonary vessels. However, these treatment options are unable to stop the progression of, or reverse, an already established disease. Recent studies have advanced a metabolic dysregulation, featuring increased glutamine metabolism, as a mechanism driving PAH progression. Metabolic dysregulation in PAH leads to increased glutaminolysis to produce substrate to meet the high-energy requirement by hyperproliferative and apoptosis-resistant pulmonary vascular cells. This article explores the role of glutamate metabolism in PAH and how it could be targeted as an anti-remodeling therapeutic strategy.
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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.