ArticleExperimental and clinical cardiology2003
Role of mitogen-activated protein kinase in cardiac hypertrophy and heart failure.
Article in Experimental and clinical cardiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
70 citing papers in PubMed, 1 synthesis or guideline pooled it, 128 citations in OpenAlex.
- Multi-ancestry genetic architecture of heart failure subtypes.Nature communications · 2026Pooled it
- VITAGRAPH: building a knowledge graph for biologically relevant learning tasks.Scientific data · 2026Article
- P2X7 receptors promote atrial remodeling and atrial fibrillation susceptibility via reactive oxygen species-mediated mitogen-activated protein kinase signaling activation.Journal of cell communication and signaling · 2026Article
- Cardiac mechanotransduction from development to disease.APL bioengineering · 2026Review
- Identification of altered salivary microRNAs in Cavalier King Charles Spaniels affected by mitral valve disease at different ACVIM stages.Scientific reports · 2026Article
- Cardiac hypertrophy at the crossroads: Mechanistic insights and emerging multimodal therapeutic strategies.European journal of pharmacology · 2025Review
- Cardiac-specific overexpression of serum response factor regulates age-associated decline in mitochondrial function.GeroScience · 2025Article
- Targeting Metabolic Dysregulation in Obesity and Metabolic Syndrome: The Emerging Role of N-Acetylcysteine.Metabolites · 2025Review
- MAPK, PI3K/Akt Pathways, and GSK-3β Activity in Severe Acute Heart Failure in Intensive Care Patients: An Updated Review.Journal of cardiovascular development and disease · 2025Review
- Implications of Oxidative Stress in the Pathophysiological Pathways of Heart Failure.International journal of molecular sciences · 2025Review
- Signalling pathways involved in urotensin II induced ventricular myocyte hypertrophy.PloS one · 2025Article
- Salt sensitivity and myocardial fibrosis: unraveling the silent cardiovascular remodeling.Frontiers in pharmacology · 2025Review
- Behavior of Hypertrophied Right Ventricle during the Development of Left Ventricular Failure Due to Myocardial Infarction.International journal of molecular sciences · 2024Review
- Protein-protein interaction network-based integration of GWAS and functional data for blood pressure regulation analysis.Human genomics · 2024Article
- Evaluation of Tyrosine Kinase Inhibitors Loaded Injectable Hydrogels for Improving Connexin43 Gap Junction Intercellular Communication.ACS applied materials & interfaces · 2024Article
- Activation of MEK-ERK-c-MYC signaling pathway promotes splenic M2-like macrophage polarization to inhibit PHcH-liver cirrhosis.Frontiers in immunology · 2024Article
- Exploring the Regulation and Function ofGenes · 2023Article
- Traditional Therapeutics and Potential Epidrugs for CVD: Why Not Both?Life (Basel, Switzerland) · 2023Review
- The Impacts of Animal-Based Diets in Cardiovascular Disease Development: A Cellular and Physiological Overview.Journal of cardiovascular development and disease · 2023Review
- Cardiac Plin5 interacts with SERCA2 and promotes calcium handling and cardiomyocyte contractility.Life science alliance · 2023Article
10 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMitogen-activated protein kinases (MAPKs) are involved in the regulation of various cellular responses including cell proliferation, differentiation and survival. Although MAPKs are activated by MAPK kinase and inactivated by phosphatases, different types of MAPKs, including extracellular signal-regulated kinases (ERK1 and 2), c-jun N-terminal protein kinases (JNK) and p38 kinases are known to participate in different signalling pathways. This article will review some salient features of the regulation and function of different forms of MAPKs in the heart. Furthermore, the status of cardiac MAPKs under different pathophysiological conditions will be described. OBSERVATIONS: A wide variety of external stimuli are known to activate MAPKs, which are then translocated from the cytoplasm to the nucleus and regulate cardiac gene expression by phosphorylating various transcriptional factors. By virtue of the involvement of ERK1/2 in hypertrophic response and of the stress-activated JNKs and p38 kinases in the process of apoptosis, MAPKs are considered to be intimately involved in cardiac remodelling. Both growth factors and phorbol esters have been shown to strongly activate ERK1/2, whereas the activation of JNKs and p38 kinases by these agents is weak. Although ischemia-reperfusion activates all types of MAPKs, JNKs and p38 kinases are mainly proapoptotic, whereas ERK1/2 are antiapoptotic.
conclusionsThe activation of ERK1/2 is involved in signal transduction pathways associated with cardiac hypertrophy; however, the exact status of MAPKs in heart failure remains to be clearly defined. While both JNKs and p38 kinases appear to participate in the genesis of ischemia-reperfusion injury, ERK1/2 are considered to be cytoprotective.
Indexed as
Identifiers
19649217PMC2719157W295353521What OpenQuestion holds
Registered trials
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.