Evidence map›Paper›PMID 27250825›Full record

ReviewBritish journal of pharmacology2017

Anti-fibrotic actions of relaxin.

C S Samuel, S G Royce, T D Hewitson, K M Denton, T E Cooney, R G Bennett

Erratum issuedOpen access · bronzeAbstract readReview
In one paragraph

Review in British journal of pharmacology, 2017. 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 73 papers.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed
11.8field-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

73 citing papers in PubMed, 127 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Relaxin-2 drives regenerative healing and suppresses scar formation.bioRxiv : the preprint server for biology · 2025
    Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 5 institutions in 2 countries.

C S SamuelCardiovascular Disease Program, Biomedicine Discovery Institute and Department of Pharmacology, Monash University, Melbourne, Vic., Australia.
S G RoyceCardiovascular Disease Program, Biomedicine Discovery Institute and Department of Pharmacology, Monash University, Melbourne, Vic., Australia.
T D HewitsonDepartment of Nephrology, Royal Melbourne Hospital, Melbourne, Vic., Australia.
K M DentonCardiovascular Disease Program, Biomedicine Discovery Institute and Department of Physiology, Monash University, Melbourne, Vic., Australia.
T E CooneyUniversity of Pittsburgh Medical Centre (UPMC) Hamot, Erie, PA, USA.
R G BennettResearch Service 151, VA Nebraska-Western Iowa Health Care System, Omaha, NE, USA.
Monash University · AUDiscovery Institute · USNebraska Medical Center · USThe Royal Melbourne Hospital · AUUPMC Hamot · US

Funding

RELAXIN FAMILY PEPTIDES AND HEPATIC FIBROSISR01AA015509 · NIAAA · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI BENNETT, ROBERT G · 2007 to 2009
$704k
Relaxin and PPAR gamma Activation for Liver Disease TreatmentI01BX000849 · VA · OMAHA VA MEDICAL CENTER · PI BENNETT, ROBERT G · 2011 to 2019
–
BLRD VA I01 BX000849NIAAA NIH HHS R01 AA015509
6 · The paper itself

Abstract

Fibrosis refers to the hardening or scarring of tissues that usually results from aberrant wound healing in response to organ injury, and its manifestations in various organs have collectively been estimated to contribute to around 45-50% of deaths in the Western world. Despite this, there is currently no effective cure for the tissue structural and functional damage induced by fibrosis-related disorders. Relaxin meets several criteria of an effective anti-fibrotic based on its specific ability to inhibit pro-fibrotic cytokine and/or growth factor-mediated, but not normal/unstimulated, fibroblast proliferation, differentiation and matrix production. Furthermore, relaxin augments matrix degradation through its ability to up-regulate the release and activation of various matrix-degrading matrix metalloproteinases and/or being able to down-regulate tissue inhibitor of metalloproteinase activity. Relaxin can also indirectly suppress fibrosis through its other well-known (anti-inflammatory, antioxidant, anti-hypertrophic, anti-apoptotic, angiogenic, wound healing and vasodilator) properties. This review will outline the organ-specific and general anti-fibrotic significance of exogenously administered relaxin and its mechanisms of action that have been documented in various non-reproductive organs such as the cardiovascular system, kidney, lung, liver, skin and tendons. In addition, it will outline the influence of sex on relaxin's anti-fibrotic actions, highlighting its potential as an emerging anti-fibrotic therapeutic. LINKED ARTICLES: This article is part of a themed section on Recent Progress in the Understanding of Relaxin Family Peptides and their Receptors. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v174.10/issuetoc.

Indexed as

CytokinesFibrosisHumansIntercellular Signaling Peptides and ProteinsRelaxinCytokinesIntercellular Signaling Peptides and ProteinsRelaxin

Identifiers

PMID27250825
PMCPMC5406285
OpenAlexW2411211573

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.