Evidence map›Paper›PMID 31602405›Full record

ArticleCommunications biology2019

SR9009 administered for one day after myocardial ischemia-reperfusion prevents heart failure in mice by targeting the cardiac inflammasome.

Cristine J Reitz, Faisal J Alibhai, Tarak N Khatua, Mina Rasouli, Byram W Bridle, Thomas P Burris, Tami A Martino

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Communications biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
11.2field-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

75 citing papers in PubMed, 114 citations in OpenAlex.

  1. The circadian clock controls hepatic stellate cell activation via a BMAL1/CK1ε/REV-ERBα/transgelin signaling pathway.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  8. Research Progress of BMAL1 in Heart Failure.Journal of the American Heart Association · 2025
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15 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

7 authors at 2 institutions in 2 countries.

Cristine J Reitz1Centre for Cardiovascular Investigations, Department of Biomedical Sciences, University of Guelph, Guelph, Ontario N1G2W1 Canada.
Faisal J Alibhai1Centre for Cardiovascular Investigations, Department of Biomedical Sciences, University of Guelph, Guelph, Ontario N1G2W1 Canada.
Tarak N Khatua1Centre for Cardiovascular Investigations, Department of Biomedical Sciences, University of Guelph, Guelph, Ontario N1G2W1 Canada.
Mina Rasouli1Centre for Cardiovascular Investigations, Department of Biomedical Sciences, University of Guelph, Guelph, Ontario N1G2W1 Canada.
Byram W Bridle2Department of Pathobiology, University of Guelph, Guelph, Ontario N1G2W1 Canada.
Thomas P Burris3Center for Clinical Pharmacology, Washington University School of Medicine and St. Louis College of Pharmacy, St. Louis, MO 63104 USA.
Tami A Martino1Centre for Cardiovascular Investigations, Department of Biomedical Sciences, University of Guelph, Guelph, Ontario N1G2W1 Canada.ORCID 0000-0003-1913-8416
University of Guelph · CAUniversity of Health Sciences and Pharmacy · US

Funding

CIHR
6 · The paper itself

Abstract

Reperfusion of patients after myocardial infarction (heart attack) triggers cardiac inflammation that leads to infarct expansion and heart failure (HF). We previously showed that the circadian mechanism is a critical regulator of reperfusion injury. However, whether pharmacological targeting using circadian medicine limits reperfusion injury and protects against HF is unknown. Here, we show that short-term targeting of the circadian driver REV-ERB with SR9009 benefits long-term cardiac repair post-myocardial ischemia reperfusion in mice. Gain and loss of function studies demonstrate specificity of targeting REV-ERB in mice. Treatment for just one day abates the cardiac NLRP3 inflammasome, decreasing immunocyte recruitment, and thereby allowing the vulnerable infarct to heal. Therapy is given in vivo, after reperfusion, and promotes efficient repair. This study presents downregulation of the cardiac inflammasome in fibroblasts as a cellular target of SR9009, inviting more targeted therapeutic investigations in the future.

Indexed as

Myocardial ReperfusionAnimalsBiomarkersBiopsyHeart FailureImmunohistochemistryInflammasomesMiceMyocardial IschemiaNLR Family, Pyrin Domain-Containing 3 ProteinNuclear Receptor Subfamily 1, Group D, Member 1PyrrolidinesThiophenesBiomarkersInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinNr1d1 protein, mouseNuclear Receptor Subfamily 1, Group D, Member 1PyrrolidinesSR9009ThiophenesCardiovascular diseasesHeart failure

Identifiers

PMID31602405
PMCPMC6776554
OpenAlexW2978966259

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.