Evidence map›Paper›PMID 30660699›Full record

ReviewMolecular and cellular endocrinology2019

Relaxin and extracellular matrix remodeling: Mechanisms and signaling pathways.

Hooi Hooi Ng, Matthew Shen, Chrishan S Samuel, Jens Schlossmann, Robert G Bennett

Open access · greenAbstract readReview
In one paragraph

Review in Molecular and cellular endocrinology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
6.2field-weighted citation impact, top 4% 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

39 citing papers in PubMed, 70 citations in OpenAlex.

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  8. Insights into the Therapeutic Targets and Molecular Mechanisms ofPharmaceuticals (Basel, Switzerland) · 2025
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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

5 authors at 4 institutions in 3 countries.

Hooi Hooi NgDepartment of Human and Molecular Genetics, Herbert Wertheim College of Medicine, Florida International University, Miami, FL, USA. Electronic address: hoong@fiu.edu.
Matthew ShenCardiovascular Disease Theme, Monash Biomedicine Discovery Institute and Department of Pharmacology, Monash University, Clayton, VIC, Australia. Electronic address: matthew.shen@monash.edu.
Chrishan S SamuelCardiovascular Disease Theme, Monash Biomedicine Discovery Institute and Department of Pharmacology, Monash University, Clayton, VIC, Australia. Electronic address: chrishan.samuel@monash.edu.
Jens SchlossmannDepartment of Pharmacology and Toxicology, Institute of Pharmacy, University Regensburg, Regensburg, Germany. Electronic address: jens.schlossmann@chemie.uni-regensburg.de.
Robert G BennettResearch Service, VA Nebraska-Western Iowa Health Care System, Departments of Internal Medicine and Biochemistry & Molecular Biology, University of Nebraska Medical Center, Omaha, NE, USA. Electronic address: rgbennet@unmc.edu.
Discovery Institute · USFlorida International University · USNebraska Medical Center · USUniversity of Regensburg · DE

Funding

Relaxin and PPAR gamma Activation for Liver Disease TreatmentI01BX000849 · VA · OMAHA VA MEDICAL CENTER · PI BENNETT, ROBERT G · 2011 to 2019
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BLRD VA I01 BX000849
6 · The paper itself

Abstract

Fibrosis is associated with accumulation of excess fibrillar collagen, leading to tissue dysfunction. Numerous processes, including inflammation, myofibroblast activation, and endothelial-to-mesenchymal transition, play a role in the establishment and progression of fibrosis. Relaxin is a peptide hormone with well-known antifibrotic properties that result from its action on numerous cellular targets to reduce fibrosis. Relaxin activates multiple signal transduction pathways as a mechanism to suppress inflammation and myofibroblast activation in fibrosis. In this review, the general mechanisms underlying fibrotic diseases are described, along with the current state of knowledge regarding cellular targets of relaxin. Finally, an overview is presented summarizing the signaling pathways activated by relaxin and other relaxin family peptide receptor agonists to suppress fibrosis.

Indexed as

Signal TransductionAnimalsExtracellular MatrixFibrosisHumansMyofibroblastsNitric OxideRelaxinNitric OxideRelaxincGMPFibrosisNitric oxideRelaxinRelaxin family peptidereceptorRelaxin family peptides

Identifiers

PMID30660699
PMCPMC7384500
OpenAlexW2909946668

What OpenQuestion holds

Textmetadata
LicenceTDM
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.