Signalling via stress-activated mitogen-activated protein kinases in the cardiovascular system.
A number of physiological, pharmacological and pathological stimuli initiate cardiac hypertrophy. The intracellular signalling events activated by these stimuli are equally complex. Our ability to treat the hypertrophic and failing myocardium effectively will require clarification of which signalling events regulate growth, remodelling and failure. Much recent attention has focused on the regulation of the mitogen-activated protein kinase cascades (MAPKs), with the importance of these cascades in the development of cardiovascular diseases being extensively explored. These signalling pathways may provide one link from the diverse stress and pharmacological extracellular stimuli to the regulation of gene expression, contractile protein regulation and protein function. This review focuses on the recent progress made in the understanding of the regulation and function of MAPKs in the cardiovascular system, with particular emphasis being placed on the events in the cardiac ventricular myocyte.
Bogoyevitch
M A
MA
Department of Biochemistry, University of Western Australia, Nedlands, Australia. marieb@cyllene.uwa.edu.au
D000818:Animals; D006332:Cardiomegaly / Q000503:physiopathology; D002320:Cardiovascular Physiological Phenomena; D004789:Enzyme Activation; D006801:Humans; D020928:Mitogen-Activated Protein Kinases / Q000502:physiology*; D008955:Models, Cardiovascular; D018121:Receptors, Cytokine / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology*; D013314:Stress, Mechanical; D013379:Substrate Specificity
D018121:Receptors, Cytokine; D020928:Mitogen-Activated Protein Kinases