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Open AccessJournal ArticleDOI

The role of inflammatory cytokines in endothelial dysfunction

Cuihua Zhang
- 03 Jul 2008 - 
- Vol. 103, Iss: 5, pp 398-406
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TLDR
The focus of this review is to summarize recent evidence showing the effects of inflammation on vascular dysfunction in ischemic-heart disease, which may prompt new directions for targeting inflammation in future therapies.
Abstract
Clinical and experimental data support a link between endothelial dysfunction and inflammation. Inflammatory cytokines are important protagonists in formation of atherosclerotic plaque, eliciting effects throughout the atherosclerotic vessel. Importantly, the development of atherosclerotic lesions, regardless of the risk factor, e.g., diabetes, hypertension, obesity, is characterized by disruption in normal function of the endothelial cells. Endothelial cells, which line the internal lumen of the vasculature, are part of a complex system that regulates vasodilation and vasoconstriction, growth of vascular smooth muscle cells, inflammation, and hemostasis, maintaining a proper blood supply to tissues and regulating inflammation and coagulation. Current concepts suggest that the earliest event in atherogenesis is endothelial dysfunction, manifested by deficiencies in the production of nitric oxide (NO) and prostacyclin. The focus of this review is to summarize recent evidence showing the effects of inflammation on vascular dysfunction in ischemic-heart disease, which may prompt new directions for targeting inflammation in future therapies.

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Journal ArticleDOI

Inflammatory Cytokines in Vascular Dysfunction and Vascular Disease

TL;DR: Genetic and pharmacological tools to decrease the production of cytokines or to diminish their effects using cytokine antagonists could provide new approaches in the management of inflammatory vascular disease.
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Endothelial glycocalyx and coronary vascular permeability: the fringe benefit

TL;DR: The oncotic pressure difference pertinent to fluid homeostasis is not built up between the intravascular and the interstitial tissue spaces, but within a small protein-free zone beneath the glycocalyx surface layer, which explains why perturbation of the glyocalyx leads to a breakdown of both fluid and protein handling in the coronary vascular bed.
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Endothelial to Mesenchymal Transition Represents a Key Link in the Interaction between Inflammation and Endothelial Dysfunction

TL;DR: Current understanding on the interactions between inflammatory processes, EndMT, and endothelial dysfunction, with a focus on the mechanisms that regulate essential signaling pathways is reviewed, to provide novel therapeutic targets for the treatment of vascular diseases.
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Expression of IL-17A in human atherosclerotic lesions is associated with increased inflammation and plaque vulnerability

TL;DR: The association of IL-17A with ischemic symptoms and vulnerable plaque characteristics suggests that the pro-inflammatory cytokine IL- 17A may contribute to atherosclerosis und plaque instability.
References
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Journal ArticleDOI

Endothelial Dysfunction in Cardiovascular Diseases: The Role of Oxidant Stress

TL;DR: Accumulating evidence suggests that oxidant stress alters many functions of the endothelium, including modulation of vasomotor tone, and as the role of these various enzyme sources of ROS become clear, it will perhaps be possible to use more specific therapies to prevent their production and ultimately correct endothelial dysfunction.
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NAD(P)H Oxidase: Role in Cardiovascular Biology and Disease

TL;DR: Vascular NAD(P)H oxidases have been found to be essential in the physiological response of vascular cells, including growth, migration, and modification of the extracellular matrix and have been linked to hypertension and to pathological states associated with uncontrolled growth and inflammation, such as atherosclerosis.
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C-Reactive Protein in Healthy Subjects: Associations With Obesity, Insulin Resistance, and Endothelial Dysfunction A Potential Role for Cytokines Originating From Adipose Tissue?

TL;DR: The data suggest that adipose tissue is an important determinant of a low level, chronic inflammatory state as reflected by levels of interleukin-6, tumor necrosis factor-alpha, and C-reactive protein, and that infection with H pylori, C pneumoniae, and cytomegalovirus is not.
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Angiotensin II-mediated hypertension in the rat increases vascular superoxide production via membrane NADH/NADPH oxidase activation. Contribution to alterations of vasomotor tone.

TL;DR: Forms of hypertension associated with elevated circulating levels of angiotensin II may have unique vascular effects not shared by other forms of hypertension because they increase vascular smooth muscle .O2- production via NADH/NADPH oxidase activation.
Journal ArticleDOI

Superoxide generation by endothelial nitric oxide synthase: The influence of cofactors

TL;DR: The mechanism of superoxide generation by endothelial nitric oxide synthase (eNOS) was investigated by the electron spin resonance spin-trapping technique using 5-diethoxyphosphoryl-5-methyl-1-pyrroline N-oxide as discussed by the authors.
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