دورية أكاديمية
أعرض في EDS

The role of the paracrine/autocrine mediator endothelin-1 in regulation of cardiac contractility and growth.

التفاصيل البيبلوغرافية
العنوان: The role of the paracrine/autocrine mediator endothelin-1 in regulation of cardiac contractility and growth.
المؤلفون: Drawnel FM; Babraham Research Campus, Babraham Institute, Cambridge, UK., Archer CR, Roderick HL
المصدر: British journal of pharmacology [Br J Pharmacol] 2013 Jan; Vol. 168 (2), pp. 296-317.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't; Review
اللغة: English
بيانات الدورية: Publisher: Wiley Country of Publication: England NLM ID: 7502536 Publication Model: Print Cited Medium: Internet ISSN: 1476-5381 (Electronic) Linking ISSN: 00071188 NLM ISO Abbreviation: Br J Pharmacol Subsets: MEDLINE
أسماء مطبوعة: Publication: London : Wiley
Original Publication: London, Macmillian Journals Ltd.
مواضيع طبية MeSH: Endothelin-1/*physiology , Heart/*physiology, Animals ; Calcium/metabolism ; Cardiomegaly/metabolism ; Endothelin Receptor Antagonists ; Humans ; Myocardial Contraction ; Protein Kinases/metabolism ; Receptors, Endothelin/metabolism ; Ventricular Remodeling/physiology
مستخلص: Unlabelled: Endothelin-1 (ET-1) is a critical autocrine and paracrine regulator of cardiac physiology and pathology. Produced locally within the myocardium in response to diverse mechanical and neurohormonal stimuli, ET-1 acutely modulates cardiac contractility. During pathological cardiovascular conditions such as ischaemia, left ventricular hypertrophy and heart failure, myocyte expression and activity of the entire ET-1 system is enhanced, allowing the peptide to both initiate and maintain maladaptive cellular responses. Both the acute and chronic effects of ET-1 are dependent on the activation of intracellular signalling pathways, regulated by the inositol-trisphosphate and diacylglycerol produced upon activation of the ET(A) receptor. Subsequent stimulation of protein kinases C and D, calmodulin-dependent kinase II, calcineurin and MAPKs modifies the systolic calcium transient, myofibril function and the activity of transcription factors that coordinate cellular remodelling. The precise nature of the cellular response to ET-1 is governed by the timing, localization and context of such signals, allowing the peptide to regulate both cardiomyocyte physiology and instigate disease.
Linked Articles: This article is part of a themed section on Endothelin. To view the other articles in this section visit http://dx.doi.org/10.1111/bph.2013.168.issue-1.
(© 2012 The Authors. British Journal of Pharmacology © 2012 The British Pharmacological Society.)
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معلومات مُعتمدة: BBS/E/B/0000C116 United Kingdom BB_ Biotechnology and Biological Sciences Research Council; BBS/E/B/0000H215 United Kingdom BB_ Biotechnology and Biological Sciences Research Council; PG/11/12/28717 United Kingdom BHF_ British Heart Foundation
المشرفين على المادة: 0 (Endothelin Receptor Antagonists)
0 (Endothelin-1)
0 (Receptors, Endothelin)
EC 2.7.- (Protein Kinases)
SY7Q814VUP (Calcium)
تواريخ الأحداث: Date Created: 20120906 Date Completed: 20130617 Latest Revision: 20220316
رمز التحديث: 20231215
مُعرف محوري في PubMed: PMC3572557
DOI: 10.1111/j.1476-5381.2012.02195.x
PMID: 22946456
قاعدة البيانات: MEDLINE
الوصف
تدمد:1476-5381
DOI:10.1111/j.1476-5381.2012.02195.x