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Obesity, inflammation, and atherosclerosis.

Nature reviews. Cardiology

metabolism, immunology, T-Lymphocytes, Rupture, Risk Factors, Risk Assessment, Prognosis, pathology, drug therapy, complications, Obesity, Macrophages, Lipid Metabolism, Insulin Resistance, Inflammation Mediators, etiology, Inflammation, therapeutic use, Immunologic Factors, Immunity, Innate, Humans, Cardiovascular Agents, Atherosclerosis, Apoptosis, Anti-Inflammatory Agents, Animals, Adipocytes

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      Abstract

      Understanding of the pathophysiology of atherogenesis has evolved substantially during the last few decades. Atherosclerosis was once identified as a lipid-storage disease, but is now recognized as a subacute inflammatory condition of the vessel wall, characterized by infiltration of macrophages and T cells, which interact with one another and with cells of the arterial wall. The pathological mechanisms of obesity recapitulate many features of the inflammatory processes at work in atherosclerosis. Our current appreciation of the similarities between obesity and atherosclerosis has already fostered innovations for the diagnosis, prognosis, and prevention of these two conditions.

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      Most cited references 112

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      Atherosclerosis--an inflammatory disease.

       R. Ross,  Paul O'Byrne (1999)
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        Inflammation and metabolic disorders.

        Metabolic and immune systems are among the most fundamental requirements for survival. Many metabolic and immune response pathways or nutrient- and pathogen-sensing systems have been evolutionarily conserved throughout species. As a result, immune response and metabolic regulation are highly integrated and the proper function of each is dependent on the other. This interface can be viewed as a central homeostatic mechanism, dysfunction of which can lead to a cluster of chronic metabolic disorders, particularly obesity, type 2 diabetes and cardiovascular disease. Collectively, these diseases constitute the greatest current threat to global human health and welfare.
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          Inflammation, atherosclerosis, and coronary artery disease.

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            Author and article information

            Journal
            10.1038/nrcardio.2009.55
            19399028

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