Evidence map›Paper›PMID 24676136›Full record

ReviewMolecular medicine (Cambridge, Mass.)2014

Molecular mechanisms of pulmonary arterial remodeling.

Patrick Crosswhite, Zhongjie Sun

Open access · goldAbstract readReview
In one paragraph

Review in Molecular medicine (Cambridge, Mass.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
8.2field-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

71 citing papers in PubMed, 126 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Deciphering the Tenascin-C Nexus: A Comprehensive Review of Its Involvement in Chronic Respiratory Diseases.Pathophysiology : the official journal of the International Society for Pathophysiology · 2025
    Review
  10. Article
  11. Review
  12. Mesenchymal stem cell therapy for pulmonary hypertension: an update.Frontiers in bioengineering and biotechnology · 2025
    Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

11 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

2 authors at 1 institution in 1 country.

Patrick CrosswhiteDepartment of Physiology, College of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States of America.
Zhongjie SunDepartment of Physiology, College of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States of America.
University of Oklahoma Health Sciences Center · US

Funding

Regulation of Blood Pressure by KlothoR01HL102074 · NHLBI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI SUN, ZHONGJIE · 2011 to 2014
$2.1M
Coupling Factor 6 in Cold-induced Kidney Dysfunction and HypertensionR01HL122166 · NHLBI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI SUN, ZHONGJIE · 2015 to 2018
$1.5M
Investigation into Cold-induced Pulmonary Vascular Inflammation and DysfunctionR01HL116863 · NHLBI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI SUN, ZHONGJIE · 2013 to 2016
$1.4M
Molecular Mechanism of Arterial StiffeningR01HL105302 · NHLBI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI SUN, ZHONGJIE · 2010 to 2014
$1.4M
American Heart Association-American Stroke Association 11PRE7830040NHLBI NIH HHS HL102074NHLBI NIH HHS HL105302NHLBI NIH HHS R01 HL102074NHLBI NIH HHS R01 HL105302NHLBI NIH HHS R01 HL116863NHLBI NIH HHS R01 HL122166
6 · The paper itself

Abstract

Pulmonary arterial hypertension (PAH) is characterized by a persistent elevation of pulmonary arterial pressure and pulmonary arterial remodeling with unknown etiology. Current therapeutics available for PAH are primarily directed at reducing the pulmonary blood pressure through their effects on the endothelium. It is well accepted that pulmonary arterial remodeling is primarily due to excessive pulmonary arterial smooth muscle cell (PASMC) proliferation that leads to narrowing or occlusion of the pulmonary vessels. Future effective therapeutics will be successful in reversing the vascular remodeling in the pulmonary arteries and arterioles. The purpose of this review is to provide updated information on molecular mechanisms involved in pulmonary arterial remodeling with a focus on growth factors, transcription factors, and epigenetic pathways in PASMC proliferation. In addition, this review will highlight novel therapeutic strategies for potentially reversing PASMC proliferation.

Indexed as

AnimalsAntihypertensive AgentsCell ProliferationEpigenesis, GeneticFamilial Primary Pulmonary HypertensionHumansHypertension, PulmonaryIntercellular Signaling Peptides and ProteinsMyocytes, Smooth MusclePulmonary ArteryTranscription FactorsAntihypertensive AgentsIntercellular Signaling Peptides and ProteinsTranscription Factors

Identifiers

PMID24676136
PMCPMC4002851
OpenAlexW2181762443

What OpenQuestion holds

Textmetadata
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.