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- Sadip Pant
- Department of Medicine, University of Arkansas for Medical Sciences and Central Arkansas Veterans Healthcare System, Little Rock, AR, USA
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- Abhishek Deshmukh
- Department of Medicine, University of Arkansas for Medical Sciences and Central Arkansas Veterans Healthcare System, Little Rock, AR, USA
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- Guru S. GuruMurthy
- Department of Medicine, University of Arkansas for Medical Sciences and Central Arkansas Veterans Healthcare System, Little Rock, AR, USA
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- Naga Venkata Pothineni
- Department of Medicine, University of Arkansas for Medical Sciences and Central Arkansas Veterans Healthcare System, Little Rock, AR, USA
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- Thomas Evans Watts
- Department of Medicine, University of Arkansas for Medical Sciences and Central Arkansas Veterans Healthcare System, Little Rock, AR, USA
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- Francesco Romeo
- Department of Cardiology, University of Rome, Tor Vergata, Rome, Italy
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- Jawahar L. Mehta
- Department of Medicine, University of Arkansas for Medical Sciences and Central Arkansas Veterans Healthcare System, Little Rock, AR, USA
抄録
<jats:p> Atherogenesis has been traditionally viewed as a metabolic disease representing arterial obstruction by fatty deposits in its wall. Today, it is believed that atherogenesis involves highly specific biochemical and molecular responses with constant interactions between various cellular players. Despite the presence of inflammatory reaction in each and every step of atherosclerosis from its inception to terminal manifestation, the cause–effect relationship of these 2 processes remains unclear. In this article, we have attempted to review the role of inflammation in the development of atherosclerosis and in its major complication—coronary heart disease. </jats:p>
収録刊行物
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- Journal of Cardiovascular Pharmacology and Therapeutics
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Journal of Cardiovascular Pharmacology and Therapeutics 19 (2), 170-178, 2013-10-31
SAGE Publications