Evidence map›Paper›PMID 31042488›Full record

ReviewJournal of molecular and cellular cardiology2019

Protective transcriptional mechanisms in cardiomyocytes and cardiac fibroblasts.

Cameron S Brand, Janet K Lighthouse, Michael A Trembley

Open access · greenAbstract readReview
In one paragraph

Review in Journal of molecular and cellular cardiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.6field-weighted citation impact, top 15% 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

11 citing papers in PubMed, 19 citations in OpenAlex.

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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

3 authors at 3 institutions in 1 country.

Cameron S BrandDepartment of Pharmacology, School of Medicine, University of California - San Diego, 9500 Gilman Drive, Biomedical Sciences Building, La Jolla, CA 92093, USA. Electronic address: csbrand@ucsd.edu.
Janet K LighthouseAab Cardiovascular Research Institute, University of Rochester School of Medicine and Dentistry, 601 Elmwood Avenue, Box CVRI, Rochester, NY 14624, USA. Electronic address: Janet_Lighthouse@urmc.rochester.edu.
Michael A TrembleyDepartment of Cardiology, Boston Children's Hospital, 300 Longwood Avenue, Boston, MA 02115, USA. Electronic address: Michael.Trembley@childrens.harvard.edu.
Boston Children's Hospital · USUniversity of California, San Diego · USUniversity of Rochester · US

Funding

RESEARCH METHODS IN PEDIATRICS HEART DISEASET32HL007572 · NHLBI · CHILDREN'S HOSPITAL BOSTON · PI Sarah D DE FERRANTI, Jane W. Newburger · 1985 to 2026
$13.0M
Training In Cardiovascular Physiology & PharmacologyT32HL007444 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Ju Chen, Robert Scott Ross · 1985 to 2026
$11.1M
MULTIDISCIPLINARY TRAINING IN PULMONARY RESEARCHT32HL066988 · NHLBI · UNIVERSITY OF ROCHESTER · PI GEORAS, STEVE N, O'REILLY, MICHAEL A · 2001 to 2021
$8.1M
Cardioprotective RhoA Signaling in Mitochondrial Quality ControlF32HL140851 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BRAND, CAMERON S. · 2018 to 2018
$59k
NHLBI NIH HHS F32 HL140851NHLBI NIH HHS T32 HL007444NHLBI NIH HHS T32 HL007572NHLBI NIH HHS T32 HL066988
6 · The paper itself

Abstract

Heart failure is the leading cause of morbidity and mortality worldwide. Several lines of evidence suggest that physical activity and exercise can pre-condition the heart to improve the response to acute cardiac injury such as myocardial infarction or ischemia/reperfusion injury, preventing the progression to heart failure. It is becoming more apparent that cardioprotection is a concerted effort between multiple cell types and converging signaling pathways. However, the molecular mechanisms of cardioprotection are not completely understood. What is clear is that the mechanisms underlying this protection involve acute activation of transcriptional activators and their corresponding gene expression programs. Here, we review the known stress-dependent transcriptional programs that are activated in cardiomyocytes and cardiac fibroblasts to preserve function in the adult heart after injury. Focus is given to prominent transcriptional pathways such as mechanical stress or reactive oxygen species (ROS)-dependent activation of myocardin-related transcription factors (MRTFs) and transforming growth factor beta (TGFβ), and gene expression that positively regulates protective PI3K/Akt signaling. Together, these pathways modulate both beneficial and pathological responses to cardiac injury in a cell-specific manner.

Indexed as

Gene Expression RegulationTranscription, GeneticAnimalsFibroblastsHeart FailureHumansMyocardial InfarctionMyocytes, CardiacSignal Transductioncardiac fibroblastcardiomyocyteCardioprotectionexercisetranscription

Identifiers

PMID31042488
PMCPMC6571165
OpenAlexW2943787017

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.