Contribution of myeloperoxidase to smoking-dependent vascular inflammation
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Contribution of myeloperoxidase to smoking-dependent vascular inflammation. / Rudolph, Tanja K; Rudolph, Volker; Baldus, Stephan.
in: ANN AM THORAC SOC, Jahrgang 5, Nr. 8, 01.12.2008, S. 820-823.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - Contribution of myeloperoxidase to smoking-dependent vascular inflammation
AU - Rudolph, Tanja K
AU - Rudolph, Volker
AU - Baldus, Stephan
PY - 2008/12/1
Y1 - 2008/12/1
N2 - Smoking remains the leading cause of cardiovascular disease, accounting for almost one third of cardiac deaths in the Western industrialized countries. Atherosclerosis in general, and coronary disease in particular, is now considered an inflammatory disease. Recent research has tried to better characterize the subcellular mechanisms of smoke and nicotine on the vessel wall and circulating mediators of disease. Whereas nicotine-dependent receptor activation on endothelial cells has long been considered to elicit antiinflammatory actions, recent observations reveal that nicotine evokes close interactions between the endothelium and proinflammatory cells: namely, leukocytes. Besides monocytes and macrophages, nicotine has been shown to stimulate neutrophils, a cell species long been considered irrelevant for the progression of atherosclerotic disease. Being stimulated by nicotine, neutrophils generate reactive oxygen species and release prooxidant enzymes like myeloperoxidase, which are capable of entering the vessel wall independently. Central mechanisms by which these enzymes can modulate the structural and functional integrity of the vessel wall have been characterized and increased our understanding of neutrophil-derived changes in vascular homeostasis in response to smoking and nicotine, respectively.
AB - Smoking remains the leading cause of cardiovascular disease, accounting for almost one third of cardiac deaths in the Western industrialized countries. Atherosclerosis in general, and coronary disease in particular, is now considered an inflammatory disease. Recent research has tried to better characterize the subcellular mechanisms of smoke and nicotine on the vessel wall and circulating mediators of disease. Whereas nicotine-dependent receptor activation on endothelial cells has long been considered to elicit antiinflammatory actions, recent observations reveal that nicotine evokes close interactions between the endothelium and proinflammatory cells: namely, leukocytes. Besides monocytes and macrophages, nicotine has been shown to stimulate neutrophils, a cell species long been considered irrelevant for the progression of atherosclerotic disease. Being stimulated by nicotine, neutrophils generate reactive oxygen species and release prooxidant enzymes like myeloperoxidase, which are capable of entering the vessel wall independently. Central mechanisms by which these enzymes can modulate the structural and functional integrity of the vessel wall have been characterized and increased our understanding of neutrophil-derived changes in vascular homeostasis in response to smoking and nicotine, respectively.
KW - Acute Coronary Syndrome/physiopathology
KW - Atherosclerosis/physiopathology
KW - Humans
KW - Inflammation/physiopathology
KW - Neutrophils/physiology
KW - Peroxidase/physiology
KW - Smoking/adverse effects
U2 - 10.1513/pats.200807-063TH
DO - 10.1513/pats.200807-063TH
M3 - SCORING: Journal article
C2 - 19017736
VL - 5
SP - 820
EP - 823
JO - ANN AM THORAC SOC
JF - ANN AM THORAC SOC
SN - 1546-3222
IS - 8
ER -