ReviewBritish journal of pharmacology2015
p38 MAPK in cardioprotection - are we there yet?
Review in British journal of pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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
40 citing papers in PubMed, 71 citations in OpenAlex.
- Cardiovascular burden of long coronavirus disease: Clinical challenges and emerging biomarkers.World journal of cardiology · 2026Review
- Investigating effects of acute severe hypoxia and p38 MAPK inhibition on boldness and anxiety-like behavior in zebrafish larvae.Frontiers in behavioral neuroscience · 2026Article
- Characterizing primary and secondary senescence in vivo.Nature aging · 2025Article
- Wenyang Zhenshuai Granules inhibits cardiomyocyte apoptosis in chronic heart failure by regulating p38 MAPK signaling pathway through exosomal miR-155.Frontiers in pharmacology · 2025Article
- Possible mechanisms of SARS-CoV-2-associated myocardial fibrosis: reflections in the post-pandemic era.Frontiers in microbiology · 2024Review
- Characterization of p38α autophosphorylation inhibitors that target the non-canonical activation pathway.Nature communications · 2023Article
- Spleen tyrosine kinase (SYK) signals are implicated in cardio-cerebrovascular diseases.Heliyon · 2023Review
- Thyroid hormones act as modulators of inflammation through their nuclear receptors.Frontiers in endocrinology · 2022Review
- SIRT1 activation and its effect on intercalated disc proteins as a way to reduce doxorubicin cardiotoxicity.Frontiers in pharmacology · 2022Review
- Microarray meta-analysis reveals IL6 and p38β/MAPK11 as potential targets of hsa-miR-124 in endothelial progenitor cells: Implications for stent re-endothelization in diabetic patients.Frontiers in cardiovascular medicine · 2022Article
- Effects of Thyroid Hormone on Tissue Hypoxia: Relevance to Sepsis Therapy.Journal of clinical medicine · 2021Review
- Diversity and versatility of p38 kinase signalling in health and disease.Nature reviews. Molecular cell biology · 2021Review
- Molecular mechanisms of doxorubicin-induced cardiotoxicity: novel roles of sirtuin 1-mediated signaling pathways.Cellular and molecular life sciences : CMLS · 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
- p38δ genetic ablation protects female mice from anthracycline cardiotoxicity.American journal of physiology. Heart and circulatory physiology · 2020Article
- Overfeeding During Lactation in Rats is Associated with Cardiovascular Insulin Resistance in the Short-Term.Nutrients · 2020Article
- Connexin 43 dephosphorylation contributes to arrhythmias and cardiomyocyte apoptosis in ischemia/reperfusion hearts.Basic research in cardiology · 2019Article
- Left Ventricular Hypertrophy: Roles of Mitochondria CYP1B1 and Melatonergic Pathways in Co-Ordinating Wider Pathophysiology.International journal of molecular sciences · 2019Review
- Cardiac Fibroblast p38 MAPK: A Critical Regulator of Myocardial Remodeling.Journal of cardiovascular development and disease · 2019Review
- Connexin43 dephosphorylation at serine 282 is associated with connexin43-mediated cardiomyocyte apoptosis.Cell death and differentiation · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
PKs transfer a phosphate from ATP to the side-chain hydroxyl group of a serine, threonine or tyrosine residue of a substrate protein. This in turn can alter that protein's function; modulating fundamental cellular processes including, metabolism, transcription, growth, division, differentiation, motility and survival. PKs are subdivided into families based on homology. One such group are the stress-activated kinases, which as the name suggests, are activated in response to cellular stresses such as toxins, cytokines, mechanical deformation and osmotic stress. Members include the p38 MAPK family, which is composed of α, β, γ and δ, isoforms which are encoded by separate genes. These kinases transduce extracellular signals and coordinate the cellular responses needed for adaptation and survival. However, in cardiovascular and other disease states, these same systems can trigger maladaptive responses that aggravate, rather than alleviate, the disease. This situation is analogous to adrenergic, angiotensin and aldosterone signalling in heart failure, where inhibition is beneficial despite the importance of these hormones to homeostasis. The question is whether similar benefits could accrue from p38 inhibition? In this review, we will discuss the structure and function of p38, the history of p38 inhibitors and their use in preclinical studies. Finally, we will summarize the results of recent cardiovascular clinical trials with p38 inhibitors.
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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.