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