ReviewFrontiers in pharmacology2015
The case for inhibiting p38 mitogen-activated protein kinase in heart failure.
Review in Frontiers in pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
What it found
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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
44 citing papers in PubMed, 66 citations in OpenAlex.
- Contribution of p38 MAPK in liver fibrosis: An overview of mechanisms, signaling pathways, and therapeutic targets (Review).International journal of molecular medicine · 2026Review
- CMGC Kinases in Viral Infection and Human Disease.Pathogens (Basel, Switzerland) · 2026Review
- Causal relevance of the JAK/STAT pathway for cardioprotection via cold acclimation.Scientific reports · 2026Article
- Identification of Bioactive Ingredients and Mechanistic Pathways of Xuefu Zhuyu Decoction in Ventricular Remodeling: A Network Pharmacology, Molecular Docking and Molecular Dynamics Simulations.Current pharmaceutical design · 2026Article
- RBM25 Regulates p38 MAPK Pathway Activation via Exon 16 Skipping of MAP4K4 in a Rat Model of Post-Infarction Heart Failure.FASEB bioAdvances · 2025Article
- Inhibition of Cardiac p38 Highlights the Role of the Phosphoproteome in Heart Failure Progression.ACS omega · 2025Article
- Norepinephrine inhibits cell cycle re-entry of neonatal rat ventricular cardiomyocytes characterized by the absence of de novo nestin expression.Physiological reports · 2025Article
- Pirfenidone Prevents Heart Fibrosis during Chronic Chagas Disease Cardiomyopathy.International journal of molecular sciences · 2024Article
- Molecular and Cellular Mechanisms Underlying the Cardiac Hypertrophic and Pro-Remodelling Effects of Leptin.International journal of molecular sciences · 2024Review
- Role of Mitogen-Activated Protein (MAP) Kinase Pathways in Metabolic Diseases.Genome integrity · 2024Review
- Article
- SOX17-mediated LPAR4 expression plays a pivotal role in cardiac development and regeneration after myocardial infarction.Experimental & molecular medicine · 2023Article
- Injection of YiQiFuMai powder protects against heart failure via inhibiting p38 and ERK1/2 MAPKs activation.Pharmaceutical biology · 2022Article
- Role of apolipoprotein O in autophagy via the p38 mitogen-activated protein kinase signaling pathway in myocardial infarction.Clinics (Sao Paulo, Brazil) · 2022Article
- Type 2 Diabetes Complicated With Heart Failure: Research on Therapeutic Mechanism and Potential Drug Development Based on Insulin Signaling Pathway.Frontiers in pharmacology · 2022Review
- Diversity and versatility of p38 kinase signalling in health and disease.Nature reviews. Molecular cell biology · 2021Review
- Atypical p38 Signaling, Activation, and Implications for Disease.International journal of molecular sciences · 2021Review
- MK2-Deficient Mice Are Bradycardic and Display Delayed Hypertrophic Remodeling in Response to a Chronic Increase in Afterload.Journal of the American Heart Association · 2021Article
- Understanding the common mechanisms of heart and skeletal muscle wasting in cancer cachexia.Oncogenesis · 2021Review
- Yixin-Shu Capsules Ameliorated Ischemia-Induced Heart Failure by Restoring Trx2 and Inhibiting JNK/p38 Activation.Oxidative medicine and cellular longevity · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
This minireview discusses the evidence that the inhibition of p38 mitogen-activated protein kinases (p38 MAPKs) maybe of therapeutic value in heart failure. Most previous experimental studies, as well as past and ongoing clinical trials, have focussed on the role of p38 MAPKs in myocardial infarction and acute coronary syndromes. There is now growing evidence that these kinases are activated within the myocardium of the failing human heart and in the heart and blood vessels of animal models of heart failure. Furthermore, from a philosophical viewpoint the chronic activation of the adaptive stress pathways that lead to the activation of p38 MAPKs in heart failure is analogous to the chronic activation of the sympathetic, renin-aldosterone-angiotensin and neprilysin systems. These have provided some of the most effective therapies for heart failure. This minireview questions whether similar and synergistic advantages would follow the inhibition of p38 MAPKs.
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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.