Evidence map›Paper›PMID 33049962›Full record

ReviewInternational journal of molecular sciences2020

p38 MAPK Pathway in the Heart: New Insights in Health and Disease.

Rafael Romero-Becerra, Ayelén M Santamans, Cintia Folgueira, Guadalupe Sabio

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed, 2 pooled it
8.3field-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

83 citing papers in PubMed, 2 syntheses or guidelines pooled it, 177 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Article
  5. Article
  6. Review
  7. Article
  8. RNAi-mediated p38δ silencing mitigates anthracycline cardiotoxicity in female mice.American journal of physiology. Heart and circulatory physiology · 2026
    Article
  9. CMGC Kinases in Viral Infection and Human Disease.Pathogens (Basel, Switzerland) · 2026
    Review
  10. Article
  11. Article
  12. Chemo-/radiotherapy-induced cardiomyopathy: roles of mitochondria and endoplasmic reticulum.Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al] · 2026
    Review
  13. DNA damage and repair in cardiomyopathy: mechanisms and therapeutic opportunities.American journal of physiology. Heart and circulatory physiology · 2026
    Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Review
  19. Review
  20. Article

23 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

4 authors at 1 institution in 1 country.

Rafael Romero-BecerraCentro Nacional de Investigaciones Cardiovasculares (CNIC), 28029 Madrid, Spain.ORCID 0000-0003-3935-2647
Ayelén M SantamansCentro Nacional de Investigaciones Cardiovasculares (CNIC), 28029 Madrid, Spain.ORCID 0000-0002-9487-7238
Cintia FolgueiraCentro Nacional de Investigaciones Cardiovasculares (CNIC), 28029 Madrid, Spain.ORCID 0000-0003-3803-9149
Guadalupe SabioCentro Nacional de Investigaciones Cardiovasculares (CNIC), 28029 Madrid, Spain.ORCID 0000-0002-2822-0625
Spanish National Centre for Cardiovascular Research · ES

Funding

FP7 Ideas: European Research Council 260464Fundación BBVA IN[17]_BBM_BAS_0066Ministerio de Ciencia y Tecnología PID2019-104399RB-I00
6 · The paper itself

Abstract

The p38 mitogen-activated kinase (MAPK) family controls cell adaptation to stress stimuli. p38 function has been studied in depth in relation to cardiac development and function. The first isoform demonstrated to play an important role in cardiac development was p38α; however, all p38 family members are now known to collaborate in different aspects of cardiomyocyte differentiation and growth. p38 family members have been proposed to have protective and deleterious actions in the stressed myocardium, with the outcome of their action in part dependent on the model system under study and the identity of the activated p38 family member. Most studies to date have been performed with inhibitors that are not isoform-specific, and, consequently, knowledge remains very limited about how the different p38s control cardiac physiology and respond to cardiac stress. In this review, we summarize the current understanding of the role of the p38 pathway in cardiac physiology and discuss recent advances in the field.

Indexed as

MAP Kinase Signaling SystemAnimalsArrhythmias, CardiacCardiomegalyHeart FailureHumansIsoenzymesMyocardiump38 Mitogen-Activated Protein KinasesProtein Kinase InhibitorsRegenerationReperfusion InjuryTreatment OutcomeIsoenzymesp38 Mitogen-Activated Protein KinasesProtein Kinase InhibitorsarrhythmiahypoxiaMAPKmetabolismp38physiologysignaling

Identifiers

PMID33049962
PMCPMC7582802
OpenAlexW3091873357

What Socratic 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 Socratic graph.