ArticleJCI insight2023
Proline and glucose metabolic reprogramming supports vascular endothelial and medial biomass in pulmonary arterial hypertension.
Article in JCI insight, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 26 citations in OpenAlex.
- Metabolic Markers as Potential Risk Factors in Pulmonary Hypertension.Pulmonary circulation · 2026Article
- Mitochondrial dysfunction in endothelial senescence: implications for vascular remodeling and therapeutic strategies.Archives of pharmacal research · 2026Review
- Beyond the Vasculature: The Emerging Role of Systemic Metabolism and Immunometabolism in Pulmonary Arterial Hypertension.International journal of molecular sciences · 2026Review
- Metabolic imprinting drives epithelial memory during mucosal fungal infection.bioRxiv : the preprint server for biology · 2025Article
- Plasma Multiplatform Metabolomics Towards Evaluation of Gender Differences in Pulmonary Arterial Hypertension-A Pilot Study.Biomedicines · 2025Article
- Lipid Ratios for Diagnosis and Prognosis of Pulmonary Hypertension.American journal of respiratory and critical care medicine · 2025Article
- Non-canonical lysosomal lipolysis drives mobilization of adipose tissue energy stores with fasting.Nature communications · 2025Article
- Transgenerational associations between newborn metabolic profiles and bronchopulmonary dysplasia in neonates born to mothers with an obese phenotype.Scientific reports · 2025Article
- Natural products targeting the immune-metabolic regulatory network in pulmonary hypertension: mechanisms, classification, and therapeutic prospects.Frontiers in pharmacology · 2025Review
- Nanoscale imaging of DNA-RNA identifies transcriptional plasticity at heterochromatin.Life science alliance · 2024Article
- Ferroptosis-Mediated Inflammation Promotes Pulmonary Hypertension.Circulation research · 2024Article
- Article
- Viewing Pulmonary Arterial Hypertension Pathogenesis and Opportunities for Disease-Modifying Therapy Through the Lens of Biomass.JACC. Basic to translational science · 2024Review
- Ferroptosis Integrates Mitochondrial Derangements and Pathological Inflammation to Promote Pulmonary Hypertension.bioRxiv : the preprint server for biology · 2024Article
- Dietary intake and glutamine-serine metabolism control pathologic vascular stiffness.Cell metabolism · 2024Article
- Mediating Metabolism: Inhibition of Malic Enzyme 1 (ME1) Restores Endothelial Bioenergetics and Adenosine Signaling in Pulmonary Hypertension.Circulation · 2024Article
- Pulmonary Hypertension: A Contemporary Review.American journal of respiratory and critical care medicine · 2023Review
- Human liver single nuclear RNA sequencing implicates BMPR2, GDF15, arginine, and estrogen in portopulmonary hypertension.Communications biology · 2023Article
- Elevated CHCHD4 orchestrates mitochondrial oxidative phosphorylation to disturb hypoxic pulmonary hypertension.Journal of translational medicine · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 4 countries.
Funding
Abstract
In pulmonary arterial hypertension (PAH), inflammation promotes a fibroproliferative pulmonary vasculopathy. Reductionist studies emphasizing single biochemical reactions suggest a shift toward glycolytic metabolism in PAH; however, key questions remain regarding the metabolic profile of specific cell types within PAH vascular lesions in vivo. We used RNA-Seq to profile the transcriptome of pulmonary artery endothelial cells (PAECs) freshly isolated from an inflammatory vascular injury model of PAH ex vivo, and these data were integrated with information from human gene ontology pathways. Network medicine was then used to map all aa and glucose pathways to the consolidated human interactome, which includes data on 233,957 physical protein-protein interactions. Glucose and proline pathways were significantly close to the human PAH disease module, suggesting that these pathways are functionally relevant to PAH pathobiology. To test this observation in vivo, we used multi-isotope imaging mass spectrometry to map and quantify utilization of glucose and proline in the PAH pulmonary vasculature at subcellular resolution. Our findings suggest that elevated glucose and proline avidity underlie increased biomass in PAECs and the media of fibrosed PAH pulmonary arterioles. Overall, these data show that anabolic utilization of glucose and proline are fundamental to the vascular pathology of PAH.
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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.