ArticleMolecular and cellular biology1998
Opposing effects of Jun kinase and p38 mitogen-activated protein kinases on cardiomyocyte hypertrophy.
Article in Molecular and cellular biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
63 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The Role of microRNAs in Heart Failure: A Systematic Review.Frontiers in cardiovascular medicine · 2020Pooled it
- Inhibition of Cardiac p38 Highlights the Role of the Phosphoproteome in Heart Failure Progression.ACS omega · 2025Article
- Cell division cycle protein 42-driven activation of the MKK3/6-p38 signaling pathway participates in cardiac remodeling in mice.Cellular and molecular life sciences : CMLS · 2025Article
- α-Melanocyte-stimulating hormone alleviates pathological cardiac remodeling via melanocortin 5 receptor.EMBO reports · 2024Article
- Application of emetine in SARS-CoV-2 treatment: regulation of p38 MAPK signaling pathway for preventing emetine-induced cardiac complications.Cell cycle (Georgetown, Tex.) · 2022Article
- Integrins in cardiac hypertrophy: lessons learned from culture systems.ESC heart failure · 2021Review
- Stress-activated kinases as therapeutic targets in pancreatic cancer.World journal of gastroenterology · 2021Review
- Resistin induces cardiac fibroblast-myofibroblast differentiation through JAK/STAT3 and JNK/c-Jun signaling.Pharmacological research · 2021Article
- 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
- Ethanol Stimulation of Microglia Release Increases ERK1/2-Dependent Neuronal cPLANeurochemical research · 2020Article
- Cardiovascular Pleiotropic Effects of Natriuretic Peptides.International journal of molecular sciences · 2019Review
- Gentisic acid attenuates pressure overload-induced cardiac hypertrophy and fibrosis in mice through inhibition of the ERK1/2 pathway.Journal of cellular and molecular medicine · 2018Article
- Improved heart failure by Rhein lysinate is associated with p38MAPK pathway.Experimental and therapeutic medicine · 2018Article
- p38 MAP kinases in the heart.Gene · 2016Review
- Low-dose radiation affects cardiac physiology: gene networks and molecular signaling in cardiomyocytes.American journal of physiology. Heart and circulatory physiology · 2015Article
- Metabolic Reprogramming Is Required for Myofibroblast Contractility and Differentiation.The Journal of biological chemistry · 2015Article
- Effect of panax notoginseng saponins injection on the p38MAPK pathway in lung tissue in a rat model of hypoxic pulmonary hypertension.Chinese journal of integrative medicine · 2015Article
- The case for inhibiting p38 mitogen-activated protein kinase in heart failure.Frontiers in pharmacology · 2015Review
- Crosstalk between mitogen-activated protein kinases and mitochondria in cardiac diseases: therapeutic perspectives.Pharmacology & therapeutics · 2014Review
- α₁A-adrenergic receptors regulate cardiac hypertrophy in vivo through interleukin-6 secretion.Molecular pharmacology · 2013Article
3 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
c-Jun N-terminal protein kinase (JNK) and p38, two distinct members of the mitogen-activated protein (MAP) kinase family, regulate gene expression in response to various extracellular stimuli, yet their physiological functions are not completely understood. In this report we show that JNK and p38 exerted opposing effects on the development of myocyte hypertrophy, which is an adaptive physiological process characterized by expression of embryonic genes and unique morphological changes. In rat neonatal ventricular myocytes, both JNK and p38 were stimulated by hypertrophic agonists like endothelin-1, phenylephrine, and leukemia inhibitory factor. Expression of MAP kinase kinase 6b (EE), a constitutive activator of p38, stimulated the expression of atrial natriuretic factor (ANF), which is a genetic marker of in vivo cardiac hypertrophy. Activation of p38 was required for ANF expression induced by the hypertrophic agonists. Furthermore, a specific p38 inhibitor, SB202190, significantly changed hypertrophic morphology induced by the agonists. Surprisingly, activation of JNK led to inhibition of ANF expression induced by MEK kinase 1 (MEKK1) and the hypertrophic agonists. MEKK1-induced ANF expression was also negatively regulated by expression of c-Jun. Our results demonstrate that p38 mediates, but JNK suppresses, the development of myocyte hypertrophy.
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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.