Evidence map›Paper›PMID 24924700›Full record

ReviewPharmacology & therapeutics2014

Crosstalk between mitogen-activated protein kinases and mitochondria in cardiac diseases: therapeutic perspectives.

Sabzali Javadov, Sehwan Jang, Bryan Agostini

Abstract readReview
In one paragraph

Review in Pharmacology & therapeutics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
94citing papers in PubMed, 1 pooled it
4.3field-weighted citation impact, top 5% 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

94 citing papers in PubMed, 1 synthesis or guideline pooled it, 155 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Chemistry and Biological Activity of 11Molecules (Basel, Switzerland) · 2026
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. The role of mechanosignaling in the control of myocardial mass.American journal of physiology. Heart and circulatory physiology · 2025
    Review
  14. Phytochemical-richFrontiers in nutrition · 2025
    Article
  15. Article
  16. Review
  17. Mitochondrial Kinase Signaling for Cardioprotection.International journal of molecular sciences · 2024
    Review
  18. Article
  19. Article
  20. Article

34 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 1 institution in 1 country.

Sabzali JavadovDepartment of Physiology, School of Medicine, University of Puerto Rico, PR, USA. Electronic address: sabzali.javadov@upr.edu.
Sehwan JangDepartment of Physiology, School of Medicine, University of Puerto Rico, PR, USA.
Bryan AgostiniDepartment of Physiology, School of Medicine, University of Puerto Rico, PR, USA.
University of Puerto Rico System · PR

Funding

Mitochondrial Permeability Transition as a Target for Cardioprotection in Heart FSC1HL118669 · NHLBI · UNIVERSITY OF PUERTO RICO MED SCIENCES · PI JAVADOV, SABZALI · 2012 to 2016
$1.3M
NHLBI NIH HHS SC1 HL118669NHLBI NIH HHS SC1HL118669
6 · The paper itself

Abstract

Cardiovascular diseases cause more mortality and morbidity worldwide than any other diseases. Although many intracellular signaling pathways influence cardiac physiology and pathology, the mitogen-activated protein kinase (MAPK) family has garnered significant attention because of its vast implications in signaling and crosstalk with other signaling networks. The extensively studied MAPKs ERK1/2, p38, JNK, and ERK5, demonstrate unique intracellular signaling mechanisms, responding to a myriad of mitogens and stressors and influencing the signaling of cardiac development, metabolism, performance, and pathogenesis. Definitive relationships between MAPK signaling and cardiac dysfunction remain elusive, despite 30 years of extensive clinical studies and basic research of various animal/cell models, severities of stress, and types of stimuli. Still, several studies have proven the importance of MAPK crosstalk with mitochondria, powerhouses of the cell that provide over 80% of ATP for normal cardiomyocyte function and play a crucial role in cell death. Although many questions remain unanswered, there exists enough evidence to consider the possibility of targeting MAPK-mitochondria interactions in the prevention and treatment of heart disease. The goal of this review is to integrate previous studies into a discussion of MAPKs and MAPK-mitochondria signaling in cardiac diseases, such as myocardial infarction (ischemia), hypertrophy and heart failure. A comprehensive understanding of relevant molecular mechanisms, as well as challenges for studies in this area, will facilitate the development of new pharmacological agents and genetic manipulations for therapy of cardiovascular diseases.

Indexed as

Heart DiseasesHumansMAP Kinase Signaling SystemMitochondriaMitogen-Activated Protein Kinase 7Mitogen-Activated Protein KinasesSignal TransductionMitogen-Activated Protein Kinase 7Mitogen-Activated Protein KinasesCardiac diseasesCell signalingHeartMAPKMitochondria

Identifiers

PMID24924700
PMCPMC4185221
OpenAlexW2068766234

What OpenQuestion holds

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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.