Open AccessNeuroendocrine and oxidoreductive mechanisms of stress induced cardiovascular diseases
Author(s) -
Pajović Sb,
Radojcić Mb,
Kanazir Dt
Publication year - 2008
Publication title -
physiological research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.647
H-Index - 70
eISSN - 1802-9973
pISSN - 0862-8408
DOI - 10.33549/physiolres.931187
Subject(s) - oxidative stress , neuroscience , pathophysiology , medicine , bioinformatics , biology
The review concerns a number of basic molecular pathways thatplay a crucial role in perception, transmission, and modulation ofthe stress signals, and mediate the adaptation of the vitalprocesses in the cardiovascular system (CVS). These highlycomplex systems for intracellular transfer of information includestress hormones and their receptors, stress-activatedphosphoprotein kinases, stress-activated heat shock proteins,and antioxidant enzymes maintaining oxidoreductive homeostasisof the CVS. Failure to compensate for the deleterious effects ofstress may result in the development of differentpathophysiological states of the CVS, such as ischemia,hypertension, atherosclerosis and infarction. Stress-induceddysbalance in each of the CVS molecular signaling systems andtheir contribution to the CVS malfunctioning is reviewed. Thegeneral picture of the molecular mechanisms of the stressinduced pathophysiology in the CVS pointed out the importanceof stress duration and intensity as etiological factors, andsuggested that future studies should be complemented by thecareful insights into the individual factors of susceptibility tostress, prophylactic effects of 'healthy' life styles and beneficialaction of antioxidant-rich nutrition.