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Produced locally within the myocardium in response to diverse mechanical and neurohormonal stimuli, <jats:styled-content style=\"fixed-case\">ET<\/jats:styled-content>\u20101 acutely modulates cardiac contractility. During pathological cardiovascular conditions such as ischaemia, left ventricular hypertrophy and heart failure, myocyte expression and activity of the entire <jats:styled-content style=\"fixed-case\">ET<\/jats:styled-content>\u20101 system is enhanced, allowing the peptide to both initiate and maintain maladaptive cellular responses. Both the acute and chronic effects of <jats:styled-content style=\"fixed-case\">ET<\/jats:styled-content>\u20101 are dependent on the activation of intracellular signalling pathways, regulated by the inositol\u2010trisphosphate and diacylglycerol produced upon activation of the <jats:styled-content style=\"fixed-case\">ET<jats:sub>A<\/jats:sub><\/jats:styled-content> receptor. Subsequent stimulation of protein kinases <jats:styled-content style=\"fixed-case\">C<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">D<\/jats:styled-content>, calmodulin\u2010dependent kinase <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>, 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 <jats:styled-content style=\"fixed-case\">ET<\/jats:styled-content>\u20101 is governed by the timing, localization and context of such signals, allowing the peptide to regulate both cardiomyocyte physiology and instigate disease.<\/jats:p><\/jats:sec><jats:sec><jats:title>Linked Articles<\/jats:title><jats:p>This article is part of a themed section on Endothelin. 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