Evidence map›Paper›PMID 25412097›Full record

ArticlePloS one2014

Thymosin Beta 4 protects mice from monocrotaline-induced pulmonary hypertension and right ventricular hypertrophy.

Chuanyu Wei, Il-Kwon Kim, Li Li, Liling Wu, Sudhiranjan Gupta

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.5field-weighted citation impact, top 31% 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

10 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Tβ4-Ac-SDKP pathway: Any relevance for the cardiovascular system?Canadian journal of physiology and pharmacology · 2019
    Review
  10. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 2 countries.

Chuanyu WeiDivision of Molecular Cardiology, Department of Medicine, College of Medicine, Texas A & M Health Science Center and Scott & White, Central Texas Veterans Health Care System, Temple, Texas, United States of America.
Il-Kwon KimDivision of Molecular Cardiology, Department of Medicine, College of Medicine, Texas A & M Health Science Center and Scott & White, Central Texas Veterans Health Care System, Temple, Texas, United States of America.
Li LiDivision of Molecular Cardiology, Department of Medicine, College of Medicine, Texas A & M Health Science Center and Scott & White, Central Texas Veterans Health Care System, Temple, Texas, United States of America; Department of Physiology and Pathophysiology, Peking University Health Science Center, Beijing, China.
Liling WuDepartment of Physiology and Pathophysiology, Peking University Health Science Center, Beijing, China.
Sudhiranjan GuptaDivision of Molecular Cardiology, Department of Medicine, College of Medicine, Texas A & M Health Science Center and Scott & White, Central Texas Veterans Health Care System, Temple, Texas, United States of America.
Central Texas Veterans Health Care System · USPeking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary hypertension (PH) is a progressive vascular disease of pulmonary arteries that impedes ejection of blood by the right ventricle. As a result there is an increase in pulmonary vascular resistance and pulmonary arterial pressure causing right ventricular hypertrophy (RVH) and RV failure. The pathology of PAH involves vascular cell remodeling including pulmonary arterial endothelial cell (PAEC) dysfunction and pulmonary arterial smooth muscle cell (PASMC) proliferation. Current therapies are limited to reverse the vascular remodeling. Investigating a key molecule is required for development of new therapeutic intervention. Thymosin beta-4 (Tβ4) is a ubiquitous G-actin sequestering protein with diverse biological function and promotes wound healing and modulates inflammatory responses. However, it remains unknown whether Tβ4 has any protective role in PH. The purpose of this study is to evaluate the whether Tβ4 can be used as a vascular-protective agent. In monocrotaline (MCT)-induced PH mouse model, we showed that mice treated with Tβ4 significantly attenuated the systolic pressure and RVH, compared to the MCT treated mice. Our data revealed for the first time that Tβ4 selectively targets Notch3-Col 3A-CTGF gene axis in preventing MCT-induced PH and RVH. Our study may provide pre-clinical evidence for Tβ4 and may consider as vasculo-protective agent for the treatment of PH induced RVH.

Indexed as

AnimalsCells, CulturedCollagen Type IIIConnective Tissue Growth FactorDisease Models, AnimalEndothelial CellsHypertension, PulmonaryHypertrophy, Right VentricularInjections, IntraperitonealLungMaleMiceMonocrotalineReceptor, Notch3Receptors, NotchSignal TransductionCCN2 protein, mouseCollagen Type IIIConnective Tissue Growth FactorMonocrotalineNotch3 protein, mouseReceptor, Notch3Receptors, NotchThymosinThymosin beta(4)

Identifiers

PMID25412097
PMCPMC4239012
OpenAlexW1987445529

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.