Evidence map›Paper›PMID 25517116›Full record

ArticleNature communications2014

The switching role of β-adrenergic receptor signalling in cell survival or death decision of cardiomyocytes.

Sung-Young Shin, Taeyong Kim, Ho-Sung Lee, Jun Hyuk Kang, Ji Young Lee, Kwang-Hyun Cho, Do Han Kim

Open access · hybridAbstract read
In one paragraph

Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

40 citing papers in PubMed, 69 citations in OpenAlex.

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  8. Normalizing Input-Output Relationships of Cancer Networks for Reversion Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Article
  9. Critical transition and reversion of tumorigenesis.Experimental & molecular medicine · 2023
    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

7 authors at 2 institutions in 1 country.

Sung-Young ShinDepartment of Bio and Brain Engineering, Korea Advanced Institute of Science and Technology (KAIST), Daejeon 305-701, Korea.
Taeyong KimSchool of Life Sciences and Systems Biology Research Center, Gwangju Institute of Science and Technology (GIST), Gwangju 500-712, Korea.
Ho-Sung Lee1] Department of Bio and Brain Engineering, Korea Advanced Institute of Science and Technology (KAIST), Daejeon 305-701, Korea [2] Graduate School of Medical Science and Engineering, KAIST, Daejeon 305-701, Korea.
Jun Hyuk Kang1] Department of Bio and Brain Engineering, Korea Advanced Institute of Science and Technology (KAIST), Daejeon 305-701, Korea [2] Graduate School of Medical Science and Engineering, KAIST, Daejeon 305-701, Korea.
Ji Young LeeSchool of Life Sciences and Systems Biology Research Center, Gwangju Institute of Science and Technology (GIST), Gwangju 500-712, Korea.
Kwang-Hyun Cho1] Department of Bio and Brain Engineering, Korea Advanced Institute of Science and Technology (KAIST), Daejeon 305-701, Korea [2] Graduate School of Medical Science and Engineering, KAIST, Daejeon 305-701, Korea.
Do Han KimSchool of Life Sciences and Systems Biology Research Center, Gwangju Institute of Science and Technology (GIST), Gwangju 500-712, Korea.
Korea Advanced Institute of Science and Technology · KRGwangju Institute of Science and Technology · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

How cell fate (survival or death) is determined and whether such determination depends on the strength of stimulation has remained unclear. In this study, we discover that the cell fate of cardiomyocytes switches from survival to death with the increase of β-adrenergic receptor (β-AR) stimulation. Mathematical simulations combined with biochemical experimentation of β-AR signalling pathways show that the gradual increment of isoproterenol (a non-selective β1/β2-AR agonist) induces the switching response of Bcl-2 expression from the initial increase followed by a decrease below its basal level. The ERK1/2 and ICER-mediated feed-forward loop is the hidden design principle underlying such cell fate switching characteristics. Moreover, we find that β1-blocker treatment increases the survival effect of β-AR stimuli through the regulation of Bcl-2 expression leading to the resistance to cell death, providing new insight into the mechanism of therapeutic effects. Our systems analysis further suggests a novel potential therapeutic strategy for heart disease.

Indexed as

Signal TransductionAdrenergic beta-AgonistsAnimalsCell DeathCell SurvivalComputer SimulationCyclic AMP Response Element ModulatorFeedback, PhysiologicalGene Expression RegulationHeart VentriclesIsoproterenolMaleMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Models, CardiovascularMyocytes, CardiacAdrenergic beta-AgonistsCrem protein, ratCyclic AMP Response Element ModulatorIsoproterenolMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Proto-Oncogene Proteins c-bcl-2Receptors, Adrenergic, beta-1Receptors, Adrenergic, beta-2

Identifiers

PMID25517116
PMCPMC4284638
OpenAlexW2005083453

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.