Evidence map›Paper›PMID 20959622›Full record

ReviewPhysiological reviews2010

Mitogen-activated protein kinase signaling in the heart: angels versus demons in a heart-breaking tale.

Beth A Rose, Thomas Force, Yibin Wang

Abstract readReview
In one paragraph

Review in Physiological reviews, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 390 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
390citing papers in PubMed, 3 pooled it
16.9field-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

390 citing papers in PubMed, 3 syntheses or guidelines pooled it, 714 citations in OpenAlex.

  1. Pooled it
  2. The Role of microRNAs in Heart Failure: A Systematic Review.Frontiers in cardiovascular medicine · 2020
    Pooled it
  3. Pooled it
  4. Efficacy and Safety of ARRY-371797 inCirculation. Genomic and precision medicine · 2023
    Trial
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330 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

3 authors at 2 institutions in 1 country.

Beth A RoseDepartments of Anesthesiology, Physiology, and Medicine, David Geffen School of Medicine, Molecular Biology, Institute, University of California at Los Angeles, Los Angeles, CA 90095, USA.
Thomas Force
Yibin Wang
Thomas Jefferson University · USUniversity of California, Los Angeles · US

Funding

ROLE OF P38 MAPK AND PP2C IN ISCHEMIC INJURY AND PROTECTIONP01HL080111 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI PING, PEIPEI · 2005 to 2009
$11.6M
Novel mechanisms in ER regulation in heartR01HL070079 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI WANG, YIBIN · 2003 to 2011
$3.2M
Novel Signaling Mechanisms and Molecular Targets in the Stressed MyocardiumR01HL098954 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI PING, PEIPEI, WANG, YIBIN · 2010 to 2013
$3.0M
Novel Function and Regulatory Mechanisms of Stress Kinase p38 in HeartR01HL103205 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI WANG, YIBIN · 2010 to 2014
$1.9M
STRESS ACTIVATED MAP KINASES IN HEART FAILURER01HL062311 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI WANG, YIBIN · 2000 to 2008
$1.9M
NHLBI NIH HHS P01 HL080111NHLBI NIH HHS R01 HL062311NHLBI NIH HHS R01 HL070079NHLBI NIH HHS R01 HL098954NHLBI NIH HHS R01 HL103205
6 · The paper itself

Abstract

Among the myriad of intracellular signaling networks that govern the cardiac development and pathogenesis, mitogen-activated protein kinases (MAPKs) are prominent players that have been the focus of extensive investigations in the past decades. The four best characterized MAPK subfamilies, ERK1/2, JNK, p38, and ERK5, are the targets of pharmacological and genetic manipulations to uncover their roles in cardiac development, function, and diseases. However, information reported in the literature from these efforts has not yet resulted in a clear view about the roles of specific MAPK pathways in heart. Rather, controversies from contradictive results have led to a perception that MAPKs are ambiguous characters in heart with both protective and detrimental effects. The primary object of this review is to provide a comprehensive overview of the current progress, in an effort to highlight the areas where consensus is established verses the ones where controversy remains. MAPKs in cardiac development, cardiac hypertrophy, ischemia/reperfusion injury, and pathological remodeling are the main focuses of this review as these represent the most critical issues for evaluating MAPKs as viable targets of therapeutic development. The studies presented in this review will help to reveal the major challenges in the field and the limitations of current approaches and point to a critical need in future studies to gain better understanding of the fundamental mechanisms of MAPK function and regulation in the heart.

Indexed as

AnimalsHeartHumansMAP Kinase Signaling SystemMitogen-Activated Protein KinasesMyocardiumMitogen-Activated Protein Kinases

Identifiers

PMID20959622
PMCPMC3808831
OpenAlexW2096847688

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.