Gewählte Publikation:
SHR
Neuro
Krebs
Kardio
Lipid
Stoffw
Microb
Mangge, H; Almer, G; Truschnig-Wilders, M; Schmidt, A; Gasser, R; Fuchs, D.
Inflammation, Adiponectin, Obesity and Cardiovascular Risk.
Curr Med Chem. 2010; 17(36):4511-4520
Doi: 10.2174/092986710794183006
Web of Science
PubMed
FullText
FullText_MUG
- Führende Autor*innen der Med Uni Graz
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Mangge Harald
- Co-Autor*innen der Med Uni Graz
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Almer Gunter
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Gasser Robert
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Schmidt Albrecht
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Truschnig-Wilders Martini
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- Abstract:
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The development of atherosclerotic lesions leading to myocardial infarction (MI) or stroke encompasses a cascade of cellular and molecular events that can well be characterized as a chronic immune-mediated inflammation occurring preferentially in the biologic surrounding of the so called metabolic syndrome. Adipokines, chemokines, cytokines, and their receptors are critically involved in the initiation and perpetuation of atherosclerosis, and they play important roles at all levels in the pathogenesis of this disease. Metabolic risk profiles associated with sedentary lifestyle, obesity, especially intra-abdominal fat accumulation, insulin resistance, and dyslipidemia pave the way for a chronic, immune-mediated vascular inflammation around vascular lipid deposits. In the present article, the impact of adiponectin, monocyte and T-cell associated cytokines (with emphasis on Neopterin), individual adipose tissue - distribution and pleiotropic drug effects on the individual course of atherosclerosis and associated cardiovascular disease are reviewed.
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Adiponectin - immunology Adiponectin - metabolism
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Animals -
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Cardiovascular Diseases - immunology Cardiovascular Diseases - metabolism Cardiovascular Diseases - pathology
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Humans -
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Inflammation -
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Obesity - immunology Obesity - metabolism
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Risk Factors -
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Adiposity
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immune-mediated inflammation
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cardiovascular risk