ReviewCirculation2007
Mitogen-activated protein kinases in heart development and diseases.
Review in Circulation, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 156 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
156 citing papers in PubMed, 1 synthesis or guideline pooled it, 309 citations in OpenAlex.
- Multifunctional biomaterial platforms for blocking the fibrosis process and promoting cellular restoring effects in myocardial fibrosis therapy.Frontiers in bioengineering and biotechnology · 2022Pooled it
- Trial
- Trial
- Common variants associated with changes in levels of circulating free fatty acids after administration of glucose-insulin-potassium (GIK) therapy in the IMMEDIATE trial.The pharmacogenomics journal · 2017Trial
- Rhythms of growth: unveiling the mechanobiology behind heart maturation.The Journal of physiology · 2026Review
- TAK1 operates at the primary cilium in non-canonical TGFB/BMP signaling to control heart development.PLoS biology · 2026Article
- Review
- Deubiquitinase USP43 exacerbates myocardial ischemia-reperfusion injury by stabilizing ASK1 and activating the JNK/P38 MAPK pathway.Basic research in cardiology · 2026Article
- Genetic background is associated with distinct patterns of proarrhythmogenic remodeling leading to atrial fibrillation in pigs with ischemic heart failure.Basic research in cardiology · 2026Article
- The SGLT2 inhibitor dapagliflozin alleviates ventricular remodeling and apoptosis after myocardial infarction by inhibiting the TGF-β1 and MAPK pathways.Journal of cardiothoracic surgery · 2026Article
- Nanomicelle-Based Multi-mRNA Delivery Promotes Cardiac Repair After Myocardial Infarction.Small science · 2026Article
- Observational
- Role of P2X7 Receptor on Hypoxia-Induced Vascular Endothelial Growth Factor Gene Expression in H9c2 Rat Cardiomyocytes.Journal of cardiovascular development and disease · 2025Article
- Targeting SYK with miR-512-3p provides therapeutic potential in myocardial fibrosis.Scientific reports · 2025Article
- Targeting Mitochondrial Reactive Oxygen Species: JP4-039's Potential as a Cardiovascular Therapeutic.Journal of clinical medicine · 2025Review
- Crystal structures of the phosphorylation mimics of human cytosolic branched chain aminotransferase.Archives of biochemistry and biophysics · 2025Article
- Fibroblast growth factor 16: Molecular mechanisms, signalling crosstalk, and emerging roles in cardiac biology and metabolic regulation.Pharmacological research · 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
- The Role of the MAPK Signaling Pathway in Cardiovascular Disease: Pathophysiological Mechanisms and Clinical Therapy.International journal of molecular sciences · 2025Review
- The role of mechanosignaling in the control of myocardial mass.American journal of physiology. Heart and circulatory physiology · 2025Review
96 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
1 author at 1 institution in 1 country.
Funding
Abstract
Mitogen-activated protein (MAP) kinases belong to a highly conserved family of Ser-Thr protein kinases in the human kinome and have diverse roles in broad physiological functions. The 4 best-characterized MAP kinase pathways, ERK1/2, JNK, p38, and ERK5, have been implicated in different aspects of cardiac regulation, from development to pathological remodeling. Recent advancements in the development of kinase-specific inhibitors and genetically engineered animal models have revealed significant new insights about MAP kinase pathways in the heart. However, this explosive body of new information also has yielded many controversies about the functional role of specific MAP kinases as either detrimental promoters or critical protectors of the heart during cardiac pathological processes. These uncertainties have raised questions on whether/how MAP kinases can be targeted to develop effective therapies against heart diseases. In this review, recent studies examining the role of MAP kinase subfamilies in cardiac development, hypertrophy, and survival are summarized.
Indexed as
Identifiers
What 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.