ArticleCellular signalling2010
Effect of pressure overload-induced hypertrophy on the expression and localization of p38 MAP kinase isoforms in the mouse heart.
Article in Cellular signalling, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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.
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Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.
- Relationship between p38 signaling pathway and arsenic-induced apoptosis: a meta-analysis.Environmental geochemistry and health · 2021Pooled it
- The role of deubiquitinases in cardiovascular diseases: mechanisms and therapeutic implications.Frontiers in cardiovascular medicine · 2025Review
- ERK3 is involved in regulating cardiac fibroblast function.Physiological reports · 2024Article
- Notch1 Is Involved in Physiologic Cardiac Hypertrophy of Mice via the p38 Signaling Pathway after Voluntary Running.International journal of molecular sciences · 2023Article
- Recent Advances of Pyridinone in Medicinal Chemistry.Frontiers in chemistry · 2022Review
- 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
- p38 MAPK Pathway in the Heart: New Insights in Health and Disease.International journal of molecular sciences · 2020Review
- p38γ MAPK contributes to left ventricular remodeling after pathologic stress and disinhibits calpain through phosphorylation of calpastatin.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Cardiac Fibroblast p38 MAPK: A Critical Regulator of Myocardial Remodeling.Journal of cardiovascular development and disease · 2019Review
- Protective transcriptional mechanisms in cardiomyocytes and cardiac fibroblasts.Journal of molecular and cellular cardiology · 2019Review
- MK5 haplodeficiency decreases collagen deposition and scar size during post-myocardial infarction wound repair.American journal of physiology. Heart and circulatory physiology · 2019Article
- Evolving concepts in the pathogenesis of uraemic cardiomyopathy.Nature reviews. Nephrology · 2019Review
- Cardiac fibroblast-specific p38α MAP kinase promotes cardiac hypertrophy via a putative paracrine interleukin-6 signaling mechanism.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- MYC dephosphorylation by the PP1/PNUTS phosphatase complex regulates chromatin binding and protein stability.Nature communications · 2018Article
- Article
- Mitogen-Activated Protein Kinase and Intracellular Polyamine Signaling Is Involved in TRPV1 Activation-Induced Cardiac Hypertrophy.Journal of the American Heart Association · 2016Article
- p38γ and δ promote heart hypertrophy by targeting the mTOR-inhibitory protein DEPTOR for degradation.Nature communications · 2016Article
- The Stress-Response MAP Kinase Signaling in Cardiac Arrhythmias.Reviews of physiology, biochemistry and pharmacology · 2016Review
- ET-1 Promotes Differentiation of Periodontal Ligament Stem Cells into Osteoblasts through ETR, MAPK, and Wnt/β-Catenin Signaling Pathways under Inflammatory Microenvironment.Mediators of inflammation · 2016Article
- p38 MAPK in cardioprotection - are we there yet?British journal of pharmacology · 2015Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
p38 mitogen-activated protein kinases (MAPKs) are serine/threonine specific protein kinases that respond to cellular stress and regulate a broad range of cellular activities. There are four major isoforms of p38 MAPK: alpha, beta, gamma, and delta. To date, the prominent isoform in heart has been thought to be p38alpha. We examined the expression of each p38 isoform at both the mRNA and protein level in murine heart. mRNA for all four p38 isoforms was detected. p38gamma and p38delta were expressed at protein levels comparable to p38alpha and 38beta, respectively. In the early phase of pressure-overload hypertrophy (1-7 days after constriction of the transverse aorta), the abundance of p38beta, p38gamma and p38delta mRNA increased; however, no corresponding changes were detected at the protein level. Confocal immunofluorescence studies revealed p38alpha and p38gamma in both the cytoplasm and nucleus. In the established phase of hypertrophy induced by chronic pressure overload (7-28 days after constriction of the transverse aorta), p38gamma immunoreactivity accumulated in the nucleus whereas the distribution of p38alpha remained unaffected. Hence, both p38alpha and p38gamma are prominent p38 isoforms in heart and p38gamma may play a role in mediating the changes in gene expression associated with cardiac remodeling during pressure-overload hypertrophy.
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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.