ArticleThe Journal of clinical investigation1998
Role of the stress-activated protein kinases in endothelin-induced cardiomyocyte hypertrophy.
Article in The Journal of clinical investigation, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 195 citations in OpenAlex.
- The Role of PKC-MAPK Signalling Pathways in the Development of Hyperglycemia-Induced Cardiovascular Complications.International journal of molecular sciences · 2022Review
- Endothelin-1 axes in the framework of predictive, preventive and personalised (3P) medicine.The EPMA journal · 2021Review
- Antihypertensive activity of a new c-Jun N-terminal kinase inhibitor in spontaneously hypertensive rats.Hypertension research : official journal of the Japanese Society of Hypertension · 2020Article
- JNK and cardiometabolic dysfunction.Bioscience reports · 2019Review
- Mixed lineage kinase-3 prevents cardiac dysfunction and structural remodeling with pressure overload.American journal of physiology. Heart and circulatory physiology · 2019Article
- PP2A negatively regulates the hypertrophic response by dephosphorylating HDAC2 S394 in the heart.Experimental & molecular medicine · 2018Article
- MicroRNA-200c modulates DUSP-1 expression in diabetes-induced cardiac hypertrophy.Molecular and cellular biochemistry · 2017Article
- Cytosolic phospholipase A2α regulates G1 progression through modulating FOXO1 activity.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
- Electrical and mechanical stimulation of cardiac cells and tissue constructs.Advanced drug delivery reviews · 2016Review
- A pathway and network review on beta-adrenoceptor signaling and beta blockers in cardiac remodeling.Heart failure reviews · 2014Review
- Crosstalk between mitogen-activated protein kinases and mitochondria in cardiac diseases: therapeutic perspectives.Pharmacology & therapeutics · 2014Review
- Role of mitogen-activated protein kinase pathways in multifactorial adverse cardiac remodeling associated with metabolic syndrome.Mediators of inflammation · 2013Review
- The role of the paracrine/autocrine mediator endothelin-1 in regulation of cardiac contractility and growth.British journal of pharmacology · 2013Review
- Characterization of hsp27 kinases activated by elevated aortic pressure in heart.Molecular and cellular biochemistry · 2012Article
- JNK modulates FOXO3a for the expression of the mitochondrial death and mitophagy marker BNIP3 in pathological hypertrophy and in heart failure.Cell death & disease · 2012Article
- Article
- The effect of adrenalectomy on the cardiac response to subacute fetal anemia.Canadian journal of physiology and pharmacology · 2011Article
- Garlic Oil Alleviates MAPKs- and IL-6-mediated Diabetes-related Cardiac Hypertrophy in STZ-induced DM Rats.Evidence-based complementary and alternative medicine : eCAM · 2011Article
- Mitogen-activated protein kinase signaling in the heart: angels versus demons in a heart-breaking tale.Physiological reviews · 2010Review
- Endothelin-1 and transforming growth factor-beta1 independently induce fibroblast resistance to apoptosis via AKT activation.American journal of respiratory cell and molecular biology · 2009Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
The signal transduction pathways governing the hypertrophic response of cardiomyocytes are not well defined. Constitutive activation of the stress-activated protein kinase (SAPK) family of mitogen-activated protein (MAP) kinases or another stress-response MAP kinase, p38, by overexpression of activated mutants of various components of the pathways is sufficient to induce a hypertrophic response in cardiomyocytes, but it is not clear what role these pathways play in the response to physiologically relevant hypertrophic stimuli. To determine the role of the SAPKs in the hypertrophic response, we used adenovirus-mediated gene transfer of SAPK/ERK kinase-1 (KR) [SEK-1(KR)], a dominant inhibitory mutant of SEK-1, the immediate upstream activator of the SAPKs, to block signal transmission down the SAPK pathway in response to the potent hypertrophic agent, endothelin-1 (ET-1). SEK-1(KR) completely inhibited ET-1-induced SAPK activation without affecting activation of the other MAP kinases implicated in the hypertrophic response, p38 and extracellular signal-regulated protein kinases (ERK)-1/ERK-2. Expression of SEK-1(KR) markedly inhibited the ET-1-induced increase in protein synthesis. In contrast, the MAPK/ERK kinase inhibitor, PD98059, which blocks ERK activation, and the p38 inhibitor, SB203580, had no effect on ET-1-induced protein synthesis. ET-1 also induced a significant increase in atrial natriuretic factor mRNA expression as well as in the percentage of cells with highly organized sarcomeres, responses which were also blocked by expression of SEK-1(KR). In summary, inhibiting activation of the SAPK pathway abrogated the hypertrophic response to ET-1. These data are the first demonstration that the SAPKs are necessary for the development of agonist-induced cardiomyocyte hypertrophy, and suggest that in response to ET-1, they transduce critical signals governing the hypertrophic response.
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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.