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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
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Führende Autor*innen der Med Uni Graz
Mangge Harald
Co-Autor*innen der Med Uni Graz
Almer Gunter
Gasser Robert
Schmidt Albrecht
Truschnig-Wilders Martini
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Abstract:
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.
Find related publications in this database (using NLM MeSH Indexing)
Adiponectin - immunology Adiponectin - metabolism
Animals -
Cardiovascular Diseases - immunology Cardiovascular Diseases - metabolism Cardiovascular Diseases - pathology
Humans -
Inflammation -
Obesity - immunology Obesity - metabolism
Risk Factors -

Find related publications in this database (Keywords)
Adiposity
immune-mediated inflammation
cardiovascular risk
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