On the origin of cardiovascular complications of sleep apnea syndrome by the means of molecular interactions.
In this article we present a novel hypothesis of the pathogenesis of cardiovascular complications of sleep apnea syndrome (SAS). Chronic intermittent hypoxia occurring in association with SAS represents a variation of chronic ischaemia reperfusion injury of the heart. In the hypoxic cells hypoxia inducible factor induces adaptation processes, including production of vascular endothelial growth factor and suppression of antioxidative mechanisms. Resulting oxidative and carbonyl stress are responsible for endothelial dysfunction leading to the development of systemic hypertension. Metabolic and vascular changes stimulate the atherogenic process. Besides the pathogenetic pathway of cardiovascular complications of SAS, we also present the latest concluding results from experimental observations and epidemiological studies concerning sleep disordered breathing and diseases of heart and vessels. Our theoretical assumption should be further proved.
Jurkovicova
I
I
1st Department of Internal Medicine, Faculty Hospital, Bratislava, Slovakia.
Celec
P
P
Mucska
I
I
Hodosy
J
J
D002319:Cardiovascular System / Q000503:physiopathology*; D004268:DNA-Binding Proteins / Q000502:physiology; D006439:Hemodynamics; D006801:Humans; D051793:Hypoxia-Inducible Factor 1; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D009687:Nuclear Proteins / Q000502:physiology; D018384:Oxidative Stress; D012891:Sleep Apnea Syndromes / Q000503:physiopathology*; D014157:Transcription Factors; D042461:Vascular Endothelial Growth Factor A / Q000502:physiology
D004268:DNA-Binding Proteins; C497442:HIF1A protein, human; D051793:Hypoxia-Inducible Factor 1; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D009687:Nuclear Proteins; D014157:Transcription Factors; D042461:Vascular Endothelial Growth Factor A