Evidence map›Paper›PMID 28637353›Full record

ReviewAntioxidants & redox signaling2018

Hallmarks of Pulmonary Hypertension: Mesenchymal and Inflammatory Cell Metabolic Reprogramming.

Angelo D'Alessandro, Karim C El Kasmi, Lydie Plecitá-Hlavatá, Petr Ježek, Min Li, Hui Zhang, Sachin A Gupte, Kurt R Stenmark

Open access · bronzeAbstract readReview
In one paragraph

Review in Antioxidants & redox signaling, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed
7.8field-weighted citation impact, top 2% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

79 citing papers in PubMed, 103 citations in OpenAlex.

  1. Trial
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  3. Response to: Comment on: The renin-angiotensin system in models of pulmonary arterial hypertension vs primary hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2026
    Article
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  7. Roles of the Altitude-Adapted Immune Microenvironment in Pulmonary Vascular Remodeling in High-Altitude Pulmonary Hypertension: A Review.Medical science monitor : international medical journal of experimental and clinical research · 2026
    Review
  8. High-Throughput Metabolomics in Transfusion Medicine.Methods in molecular biology (Clifton, N.J.) · 2026
    Article
  9. Article
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  19. Journal of the American Heart Association · 2024
    Article
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19 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Angelo D'Alessandro1 Department of Biochemistry and Molecular Genetics, University of Colorado - Denver , Colorado.
Karim C El Kasmi2 Developmental Lung Biology and Cardiovascular Pulmonary Research Laboratories, University of Colorado - Denver , Colorado.
Lydie Plecitá-Hlavatá4 Department of Mitochondrial Physiology, Institute of Physiology , Czech Academy of Sciences, Prague, Czech Republic .
Petr Ježek4 Department of Mitochondrial Physiology, Institute of Physiology , Czech Academy of Sciences, Prague, Czech Republic .
Min Li2 Developmental Lung Biology and Cardiovascular Pulmonary Research Laboratories, University of Colorado - Denver , Colorado.
Hui Zhang2 Developmental Lung Biology and Cardiovascular Pulmonary Research Laboratories, University of Colorado - Denver , Colorado.
Sachin A Gupte5 Department of Pharmacology, School of Medicine, New York Medical College , Valhalla, New York.
Kurt R Stenmark2 Developmental Lung Biology and Cardiovascular Pulmonary Research Laboratories, University of Colorado - Denver , Colorado.
Czech Academy of Sciences · CZCzech Academy of Sciences, Institute of Physiology · CZ

Funding

VRAC and Rho in pulmonary EC proliferationP01HL014985 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI STENMARK, KURT R. · 1985 to 2019
$35.1M
Fibroblasts and Mononuclear Fibrogenic Cells Drive Right Ventricular Pulmonary ArR01HL114887 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI BULL, TODD M, BUTTRICK, PETER N. · 2012 to 2016
$3.4M
Regulation of Vascular Smooth Muscle Cell Phenotype by a Novel Isoform of Glucose-6-Phosphate DehydrogenaseR01HL132574 · NHLBI · NEW YORK MEDICAL COLLEGE · PI GUPTE, SACHIN A, MIANO, JOSEPH M · 2017 to 2020
$2.5M
NHLBI NIH HHS P01 HL014985NHLBI NIH HHS R01 HL114887NHLBI NIH HHS R01 HL132574
6 · The paper itself

Abstract

significanceThe molecular events that promote the development of pulmonary hypertension (PH) are complex and incompletely understood. The complex interplay between the pulmonary vasculature and its immediate microenvironment involving cells of immune system (i.e., macrophages) promotes a persistent inflammatory state, pathological angiogenesis, and fibrosis that are driven by metabolic reprogramming of mesenchymal and immune cells. Recent Advancements: Consistent with previous findings in the field of cancer metabolism, increased glycolytic rates, incomplete glucose and glutamine oxidation to support anabolism and anaplerosis, altered lipid synthesis/oxidation ratios, increased one-carbon metabolism, and activation of the pentose phosphate pathway to support nucleoside synthesis are but some of the key metabolic signatures of vascular cells in PH. In addition, metabolic reprogramming of macrophages is observed in PH and is characterized by distinct features, such as the induction of specific activation or polarization states that enable their participation in the vascular remodeling process. CRITICAL ISSUES: Accumulation of reducing equivalents, such as NAD(P)H in PH cells, also contributes to their altered phenotype both directly and indirectly by regulating the activity of the transcriptional co-repressor C-terminal-binding protein 1 to control the proliferative/inflammatory gene expression in resident and immune cells. Further, similar to the role of anomalous metabolism in mitochondria in cancer, in PH short-term hypoxia-dependent and long-term hypoxia-independent alterations of mitochondrial activity, in the absence of genetic mutation of key mitochondrial enzymes, have been observed and explored as potential therapeutic targets. FUTURE DIRECTIONS: For the foreseeable future, short- and long-term metabolic reprogramming will become a candidate druggable target in the treatment of PH. Antioxid. Redox Signal. 28, 230-250.

Indexed as

AnimalsCarbonEnergy MetabolismEpigenesis, GeneticGene Expression RegulationGlucoseGlucosephosphate DehydrogenaseGlycolysisHumansHydrogen-Ion ConcentrationHypertension, PulmonaryHypoxiaIsoenzymesMacrophagesMitochondriaOxidation-ReductionCarbonGlucoseGlucosephosphate DehydrogenaseIsoenzymesSuperoxidesaerobic glycolysishypoxiametabolismmitochondriapulmonary hypertension

Identifiers

PMID28637353
PMCPMC5737722
OpenAlexW2636866226

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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.