Review Article | Published:

Obesity, inflammation, and atherosclerosis

Nature Reviews Cardiology volume 6, pages 399409 (2009) | Download Citation

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.

Key points

  • Although they are distinct conditions, atherosclerotic disease and obesity share common pathophysiological features

  • Lipids contribute critically to atherosclerosis and obesity; oxidized LDL and free fatty acids can trigger inflammation and initiate disease

  • Inflammation mediates all stages of atherogenesis—from early lesion development to atheroma complication—and is associated with obesity, insulin resistance, and type 2 diabetes

  • Inflammation constitutes a mechanistic link between obesity and atherosclerosis: adipokines released by adipose tissue induce insulin resistance, endothelial dysfunction, hypercoagulability, and systemic inflammation, all of which can promote atherosclerosis

  • The accumulation of heterogeneous macrophage populations, T-cell activation, cell death, and the effects of numerous cytokines and chemokines characterize both atherosclerosis and obesity

  • Inflammatory biomarkers, such as high-sensitivity C-reactive protein, can predict cardiovascular events, guide therapy, and reflect the pathophysiological links between obesity and its associated metabolic disorders

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Acknowledgements

The authors thank Joan Perry for excellent editorial assistance.

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Affiliations

  1. Division of Cardiovascular Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.

    • Viviane Z. Rocha
    •  & Peter Libby

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Competing interests

The authors declare no competing financial interests.

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Correspondence to Peter Libby.

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https://doi.org/10.1038/nrcardio.2009.55

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