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dc.creatorPajović, Snežana B.
dc.creatorRadoičić, Marija B.
dc.creatorKanazir, D. T.
dc.date.accessioned2018-03-01T20:28:17Z
dc.date.available2018-03-01T20:28:17Z
dc.date.issued2008
dc.identifier.issn0862-8408 (print)
dc.identifier.urihttp://vinar.vin.bg.ac.rs/handle/123456789/3478
dc.description.abstractThe review concerns a number of basic molecular pathways that play a crucial role in perception, transmission, and modulation of the stress signals, and mediate the adaptation of the vital processes in the cardiovascular system (CVS). These highly complex systems for intracellular transfer of information include stress hormones and their receptors, stress-activated phosphoprotein kinases, stress-activated heat shock proteins, and antioxidant enzymes maintaining oxidoreductive homeostasis of the CVS. Failure to compensate for the deleterious effects of stress may result in the development of different pathophysiological states of the CVS, such as ischemia, hypertension, atherosclerosis and infarction. Stress-induced dysbalance in each of the CVS molecular signaling systems and their contribution to the CVS malfunctioning is reviewed. The general picture of the molecular mechanisms of the stress-induced pathophysiology in the CVS pointed out the importance of stress duration and intensity as etiological factors, and suggested that future studies should be complemented by the careful insights into the individual factors of susceptibility to stress, prophylactic effects of healthy life styles and beneficial action of antioxidant-rich nutrition.en
dc.rightsrestrictedAccessen
dc.sourcePhysiological Researchen
dc.subjectneuroendocrine responseen
dc.subjectoxidative stressen
dc.subjectcardiovascular diseasesen
dc.titleNeuroendocrine and oxidoreductive mechanisms of stress-induced cardiovascular diseasesen
dc.typereviewen
dcterms.abstractКаназир, Д. Т.; Пајовиц, С. Б.; Радоичић Марија;
dc.citation.volume57
dc.citation.issue3
dc.citation.spage327
dc.citation.epage338
dc.identifier.wos000257270900003
dc.citation.rankM23
dc.identifier.pmid17465697


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