ReviewInternational journal of molecular medicine2024
Glycolysis modulation: New therapeutic strategies to improve pulmonary hypertension (Review).
Review in International journal of molecular medicine, 2024. 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
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
9 citing papers in PubMed.
- Reprogramming macrophage metabolism for cardiovascular therapy: From molecular pathways to precision nanomedicine.Materials today. Bio · 2026Review
- Myocardial fibrosis and glycolysis: a bibliometric study and visualization analysis (2000-2024).Journal of translational medicine · 2026Review
- Nicotinamide phosphoribosyltransferase activates the mitochondrial unfolded protein response to promote pulmonary arterial endothelial cell proliferation.bioRxiv : the preprint server for biology · 2026Article
- Hypoxic microenvironment and pulmonary hypertension.Respiratory research · 2025Review
- Roles of Lipid Metabolism in Pulmonary Hypertension: Friend or Foe?Biomolecules · 2025Review
- Comorbidity of hypertension and lung cancer: interplay of genetics and environment.Discover oncology · 2025Review
- Review
- LONP1 facilitates pulmonary artery smooth muscle cell glycolytic reprogramming by degrading MPC1 in pulmonary hypertension.Clinical science (London, England : 1979) · 2025Article
- Mitochondrial Dysfunction: A New Hallmark in Hereditable Thoracic Aortic Aneurysm Development.Cells · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pulmonary hypertension (PH) is a progressive life‑threatening cardiopulmonary vascular disease involving various pathological mechanisms, including hypoxia, cellular metabolism, inflammation, abnormal proliferation and apoptosis. Specifically, metabolism has attracted the most attention. Glucose metabolism is essential to maintain the cardiopulmonary vascular function. However, once exposed to a noxious stimulus, intracellular glucose metabolism changes or switches to an alternative pathway more suitable for adaptation, which is known as metabolic reprogramming. By promoting the switch from oxidative phosphorylation to glycolysis, cellular metabolic reprogramming plays an important role in PH development. Suppression of glucose oxidation and secondary upregulation of glycolysis are responsible for various features of PH, including the proliferation and apoptosis resistance of pulmonary artery endothelial and smooth muscle cells. In the present review, the roles and importance of the glucose metabolism shift were discussed to aid in the development of new treatment approaches for PH.
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.