Evidence map›Paper›PMID 24355640›Full record

ReviewJournal of the American College of Cardiology2013

Relevant issues in the pathology and pathobiology of pulmonary hypertension.

Rubin M Tuder, Stephen L Archer, Peter Dorfmüller, Serpil C Erzurum, Christophe Guignabert, Evangelos Michelakis, Marlene Rabinovitch, Ralph Schermuly, Kurt R Stenmark, Nicholas W Morrell

Abstract readReview
In one paragraph

Review in Journal of the American College of Cardiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 297 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
297citing papers in PubMed, 6 pooled it
37.9field-weighted citation impact, top 1% 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

297 citing papers in PubMed, 6 syntheses or guidelines pooled it, 568 citations in OpenAlex.

  1. Pooled it
  2. Exercise-based rehabilitation programmes for pulmonary hypertension.The Cochrane database of systematic reviews · 2023
    Pooled it
  3. Pooled it
  4. Pooled it
  5. Meta-analysis of blood genome-wide expression profiling studies in pulmonary arterial hypertension.American journal of physiology. Lung cellular and molecular physiology · 2020
    Pooled it
  6. Guideline
  7. Article
  8. Review
  9. Article
  10. Article
  11. A Paradigm Shift of HCurrent issues in molecular biology · 2026
    Review
  12. Article
  13. Review
  14. Article
  15. Article
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  17. Review
  18. Review
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  20. Article

237 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 9 institutions in 6 countries.

Rubin M TuderProgram in Translational Lung Research, Department of Medicine, University of Colorado School of Medicine, Aurora, Colorado. Electronic address: rubin.tuder@ucdenver.edu.
Stephen L ArcherDepartment of Medicine, Queen's University, Kingston, Ontario, Canada.
Peter DorfmüllerDepartment of Pathology, Marie Lannelongue Hospital, University Paris-Sud, Le Plessis-Robinson, France.
Serpil C ErzurumLerner Research Institute and Respiratory Institute, Cleveland Clinic, Cleveland, Ohio.
Christophe GuignabertINSERM UMR 999, LabEx LERMIT, Marie Lannelongue Hospital and University Paris-Sud, School of Medicine, Kremlin-Bicêtre, France.
Evangelos MichelakisDepartment of Medicine, University of Alberta, Edmonton, Alberta, Canada.
Marlene RabinovitchCardiovascular Institute and Department of Pediatrics and The Vera Moulton Wall Center for Pulmonary Vascular Disease, Stanford University School of Medicine, Stanford, California.
Ralph SchermulyExcellence Cluster Cardio-Pulmonary System, German Lung Center, Universities of Giessen and Marburg Lung Center, Justus-Liebig-University, Giessen, Germany.
Kurt R StenmarkCardiovascular Pulmonary Laboratory, Department of Pediatrics, University of Colorado School of Medicine, Aurora, Colorado.
Nicholas W MorrellDepartment of Medicine, University of Cambridge School of Clinical Medicine, Cambridge, United Kingdom. Electronic address: nwm23@cam.ac.uk.
University of Colorado Denver · USCardiovascular Institute of the South · USCleveland Clinic Lerner College of Medicine · USHôpital Marie Lannelongue · FRInserm · FRJustus-Liebig-Universität Gießen · DEQueen's University · CAUniversity of Alberta · CAUniversity of Cambridge · GB

Funding

VRAC and Rho in pulmonary EC proliferationP01HL014985 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI STENMARK, KURT R. · 1985 to 2019
$35.1M
The Cellular Response to Elafin in PAHP01HL108797 · NHLBI · STANFORD UNIVERSITY · PI RABINOVITCH, MARLENE · 2011 to 2021
$19.7M
Non-Invasive Inhaled NO in Premature NewbornsP50HL084923 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI STENMARK, KURT R. · 2007 to 2012
$11.2M
NITRIC OXIDE PRODUCTION AND REACTIONS IN THE LUNGR01HL060917 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI Serpil C. Erzurum · 1999 to 2026
$6.3M
Airway redox biochemistry as a deteriminant of asthma phenotype during adolescen*U10HL109250 · NHLBI · UNIVERSITY OF VIRGINIA · PI ERZURUM, SERPIL C., GASTON, BENJAMIN · 2011 to 2016
$4.2M
Nitric Oxide in Pulmonary HypertensionR37HL060917 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI ERZURUM, SERPIL C. · 2009 to 2018
$3.9M
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
Pulmonary Vascular-Right Ventricular Axis Research ProgramR01HL115008 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI ERZURUM, SERPIL C., PRASAD, SATHYAMANGLA V · 2012 to 2016
$3.1M
O2 sensing in the human and rabbit ductus arteriosus.R01HL071115 · NHLBI · UNIVERSITY OF CHICAGO · PI ARCHER, STEPHEN L · 2004 to 2015
$3.1M
The Role of DRP-1 and Mitochondrial Fission in Pulmonary Arterial HypertensionR01HL113003 · NHLBI · QUEEN'S UNIVERSITY AT KINGSTON · PI ARCHER, STEPHEN L · 2013 to 2016
$1.1M
Impaired mitochondrial fusion in pulmonary arterial hypertensionRC1HL099462 · NHLBI · UNIVERSITY OF CHICAGO · PI ARCHER, STEPHEN L · 2009 to 2010
$1.0M
Zipcode based nano-imaging of hypertensive pulmonary arteriesRC1HL100849 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI TUDER, RUBIN M. · 2009 to 2010
$1000k
British Heart Foundation RG/13/4/30107NHLBI NIH HHS 1R01HL114887NHLBI NIH HHS 1RC1HL099462NHLBI NIH HHS F32 HL010084NHLBI NIH HHS HL115008NHLBI NIH HHS HL60917NHLBI NIH HHS NIH PPG 5P01HL014985NHLBI NIH HHS NIH-RO1-HL071115NHLBI NIH HHS P01 HL014985NHLBI NIH HHS P01 HL108797NHLBI NIH HHS P50 HL084923NHLBI NIH HHS R01 HL060917NHLBI NIH HHS R01 HL071115NHLBI NIH HHS R01 HL113003NHLBI NIH HHS R01 HL114887NHLBI NIH HHS R01 HL115008NHLBI NIH HHS R37 HL060917NHLBI NIH HHS RC1 HL 10084NHLBI NIH HHS RC1 HL100849NHLBI NIH HHS U10 HL109250PHS HHS NIH/NHLBI SCCOR 5P50HL084923
6 · The paper itself

Abstract

Knowledge of the pathobiology of pulmonary hypertension (PH) continues to accelerate. However, fundamental gaps remain in our understanding of the underlying pathological changes in pulmonary arteries and veins in the different forms of this syndrome. Although PH primarily affects the arteries, venous disease is increasingly recognized as an important entity. Moreover, prognosis in PH is determined largely by the status of the right ventricle, rather than the levels of pulmonary artery pressures. It is increasingly clear that although vasospasm plays a role, PH is an obstructive lung panvasculopathy. Disordered metabolism and mitochondrial structure, inflammation, and dysregulation of growth factors lead to a proliferative, apoptosis-resistant state. These abnormalities may be acquired, genetically mediated as a result of mutations in bone morphogenetic protein receptor-2 or activin-like kinase-1, or epigenetically inherited (as a result of epigenetic silencing of genes such as superoxide dismutase-2). There is a pressing need to better understand how the pathobiology leads to severe disease in some patients versus mild PH in others. Recent recognition of a potential role of acquired abnormalities of mitochondrial metabolism in the right ventricular myocytes and pulmonary vascular cells suggests new therapeutic approaches, diagnostic modalities, and biomarkers. Finally, dissection of the role of pulmonary inflammation in the initiation and promotion of PH has revealed a complex yet fascinating interplay with pulmonary vascular remodeling, promising to lead to novel therapeutics and diagnostics. Emerging concepts are also relevant to the pathobiology of PH, including a role for bone marrow and circulating progenitor cells and microribonucleic acids. Continued interest in the interface of the genetic basis of PH and cellular and molecular pathogenetic links should further expand our understanding of the disease.

Indexed as

AnimalsHumansHypertension, PulmonaryMuscle, Smooth, VascularPulmonary ArteryPulmonary VeinsSignal Transductionactivin receptor-like kinaseALKBMPR2bone morphogenetic protein type II receptorDCdendritic cellendoplasmic reticulumERHIFhypoxia inducible factoridiopathic pulmonary arterial hypertensioninflammationIPAHleft heart failureLHFmetabolismPAHPHpulmonary arterial hypertensionpulmonary arteriespulmonary hypertensionpulmonary veins

Identifiers

PMID24355640
PMCPMC3970402
OpenAlexW2152216118

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.