Evidence map›Paper›PMID 31052420›Full record

ReviewInternational journal of molecular sciences2019

ERK: A Key Player in the Pathophysiology of Cardiac Hypertrophy.

Simona Gallo, Annapia Vitacolonna, Alessandro Bonzano, Paolo Comoglio, Tiziana Crepaldi

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 136 papers.

0numbers the graph read from it
0cells of the map it votes in
136citing papers in PubMed
10.9field-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

136 citing papers in PubMed, 258 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Exercise-induced cardiac hypertrophy: cellular and molecular mechanisms of cardiac adaptation following physical activity.Postepy w kardiologii interwencyjnej = Advances in interventional cardiology · 2026
    Review
  5. Review
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  9. Signaling pathways and potential therapeutic agents in trastuzumab-induced cardiotoxicity.Apoptosis : an international journal on programmed cell death · 2026
    Review
  10. Article
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  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
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  18. Article
  19. Article
  20. Article

76 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

5 authors at 3 institutions in 1 country.

Simona GalloCandiolo Cancer Institute, FPO-IRCCS, 10060 Candiolo (TO), Italy. simona.gallo@ircc.it.
Annapia VitacolonnaCandiolo Cancer Institute, FPO-IRCCS, 10060 Candiolo (TO), Italy. annapia.vitacolonna@ircc.it.
Alessandro BonzanoCandiolo Cancer Institute, FPO-IRCCS, 10060 Candiolo (TO), Italy. alessandro.bonzano@ircc.it.
Paolo ComoglioCandiolo Cancer Institute, FPO-IRCCS, 10060 Candiolo (TO), Italy. pcomoglio@gmail.com.
Tiziana CrepaldiCandiolo Cancer Institute, FPO-IRCCS, 10060 Candiolo (TO), Italy. tiziana.crepaldi@unito.it.
Candiolo Cancer Institute · ITIstituti di Ricovero e Cura a Carattere Scientifico · ITUniversity of Turin · IT

Funding

Compagnia di San Paolo ID ROL 17290Ministero della Salute "Ricerca Corrente 2018"
6 · The paper itself

Abstract

Cardiac hypertrophy is an adaptive and compensatory mechanism preserving cardiac output during detrimental stimuli. Nevertheless, long-term stimuli incite chronic hypertrophy and may lead to heart failure. In this review, we analyze the recent literature regarding the role of ERK (extracellular signal-regulated kinase) activity in cardiac hypertrophy. ERK signaling produces beneficial effects during the early phase of chronic pressure overload in response to G protein-coupled receptors (GPCRs) and integrin stimulation. These functions comprise (i) adaptive concentric hypertrophy and (ii) cell death prevention. On the other hand, ERK participates in maladaptive hypertrophy during hypertension and chemotherapy-mediated cardiac side effects. Specific ERK-associated scaffold proteins are implicated in either cardioprotective or detrimental hypertrophic functions. Interestingly, ERK phosphorylated at threonine 188 and activated ERK5 (the big MAPK 1) are associated with pathological forms of hypertrophy. Finally, we examine the connection between ERK activation and hypertrophy in (i) transgenic mice overexpressing constitutively activated RTKs (receptor tyrosine kinases), (ii) animal models with mutated sarcomeric proteins characteristic of inherited hypertrophic cardiomyopathies (HCMs), and (iii) mice reproducing syndromic genetic RASopathies. Overall, the scientific literature suggests that during cardiac hypertrophy, ERK could be a "good" player to be stimulated or a "bad" actor to be mitigated, depending on the pathophysiological context.

Indexed as

MAP Kinase Signaling SystemAnimalsCardiomegalyHumansMyocardiumadaptive and maladaptive hypertrophyanthracycline-induced cardiotoxicityERK pathwayhypertrophic cardiomyopathyRASopathiestarget therapies

Identifiers

PMID31052420
PMCPMC6539093
OpenAlexW2943156153

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.