Evidence map›Paper›PMID 29346407›Full record

ArticlePloS one2018

Relaxin reverses inflammatory and immune signals in aged hearts.

Brian Martin, Beth Ann Gabris-Weber, Rajiv Reddy, Guillermo Romero, Ansuman Chattopadhyay, Guy Salama

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.9field-weighted citation impact, top 7% 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

23 citing papers in PubMed, 45 citations in OpenAlex.

  1. Relaxin-2: Shaping the Proteomic Landscape of Skeletal Muscle Physiology, Glucose Trafficking, and Mitochondrial Function in Rat.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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  10. Relaxin does not prevent development of hypoxia-induced pulmonary edema in rats.Pflugers Archiv : European journal of physiology · 2022
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  16. HighJournal of Cancer · 2021
    Article
  17. Adipokines and Inflammation: Focus on Cardiovascular Diseases.International journal of molecular sciences · 2020
    Review
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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

6 authors at 1 institution in 1 country.

Brian MartinDepartment of Bioengineering, University of Pittsburgh, Pittsburgh, PA, United States of America.
Beth Ann Gabris-WeberSchool of Medicine, Heart and Vascular Institute, University of Pittsburgh, Pittsburgh, PA, United States of America.
Rajiv ReddySchool of Medicine, Heart and Vascular Institute, University of Pittsburgh, Pittsburgh, PA, United States of America.
Guillermo RomeroDepartment of Pharmacology & Chemical Biology, University of Pittsburgh, Pittsburgh, PA, United States of America.
Ansuman ChattopadhyayMolecular Biology Information Service, Health Sciences Library System, University of Pittsburgh, Pittsburgh, PA, United States of America.
Guy SalamaDepartment of Bioengineering, University of Pittsburgh, Pittsburgh, PA, United States of America.ORCID 0000-0002-5306-8178
University of Pittsburgh · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background'Healthy' aging drives structural and functional changes in the heart including maladaptive electrical remodeling, fibrosis and inflammation, which lower the threshold for cardiovascular diseases such as heart failure (HF) and atrial fibrillation (AF). Despite mixed results in recent clinical trials, Relaxin-therapy for 2-days could reduce mortality by 37% at 180-days post-treatment, in patients with acute decompensated HF. Relaxin's short life-span (hours) but long-lasting protective actions led us to test the hypothesis that relaxin acts at a genomic level to reverse maladaptive remodeling in aging and HF. METHODS AND

resultsYoung (9-month) and aged (24-month), male and female F-344/Brown Norway rats were treated with relaxin (0.4 mg/kg/day) for 2-weeks delivered by subcutaneous osmotic mini-pumps or with sodium acetate (controls). The genomic effects of aging and relaxin were evaluated by extracting RNA from the left ventricles and analyzing genomic changes by RNA-sequencing, Ingenuity Pathway Analysis, MetaCore and tissue immunohistochemistry. We found that aging promotes a native inflammatory response with distinct sex-differences and relaxin suppresses transcription of multiple genes and signaling pathways associated with inflammation and HF in both genders. In addition, aging significantly increased: macrophage infiltration and atrial natriuretic peptide levels in female ventricles, and activation of the complement cascade, whereas relaxin reversed these age-related effects.

conclusionThese data support the hypothesis that relaxin alters gene transcription and suppresses inflammatory pathways and genes associated with HF and aging. Relaxin's suppression of inflammation and fibrosis supports its potential as a therapy for cardiovascular and inflammation-related diseases, such as HF, AF and diabetes.

Indexed as

Disease Models, AnimalAge FactorsAgingAnimalsAtrial FibrillationBiomarkersCohort StudiesFemaleFluorescent Antibody TechniqueHeartHeart FailureHumansInflammationMacrophagesMaleRatsBiomarkersRelaxin

Identifiers

PMID29346407
PMCPMC5773192
OpenAlexW2793250092

What OpenQuestion holds

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LicenceCC BY
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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.