Article Text

Disruption of Cholesterol Efflux by Coxib Medications and Inflammatory Processes
  1. Allison B. Reiss, MD*,
  2. Farah Anwar, MD*,
  3. Edwin S.L. Chan, MD,
  4. Kamran Anwar, PhD*
  1. From the *Vascular Biology Institute, Department of Medicine, Winthrop-University Hospital, Mineola, NY, and †Department of Medicine, NYU School of Medicine, New York, NY.
  1. Received December 18, 2008, and in revised form January 29, 2009.
  2. Accepted for publication January 29, 2009.
  3. Reprints: Allison B. Reiss, MD, Vascular Biology Institute, Department of Medicine, Winthrop-University Hospital, Suite 502, 222 Station Plaza N, Mineola, NY 11501. E-mail: AReiss{at}
  4. This work was supported by an Innovative Research Grant from the Arthritis Foundation, National Center. This symposium was supported in part by a grant from the National Center for Research Resources (R13 RR023236).

Link to Increased Cardiovascular Risk


Atherosclerosis is a chronic progressive disease that is a major contributor to cardiac death. It is characterized by inflammation and cholesterol deposition in the arterial wall. Excess cholesterol accumulation occurs as a result of an imbalance between delivery and removal and leads to formation of lipid-laden foam cells. Removal of cholesterol through a process known as reverse cholesterol transport requires the coordinated functioning of a number of genes including the P450 27-hydroxylase and the adenosine triphosphate-binding cassette transporter A1 (ABCA1). Reverse cholesterol transport is a key defense against atheroma formation. This review discusses the role of inflammatory processes in impeding reverse cholesterol transport. Particular emphasis is placed on the disruption of cholesterol outflow observed in the presence of cyclooxygenase inhibitors in cultured monocytes/macrophages. These inhibitors, which are used clinically to relieve pain and inflammation, have been associated with increased risk of cardiovascular disease and myocardial infarction. We explore the relationship between suppression of reverse cholesterol transport and harmful cardiac effects of coxibs.

Key Words
  • atherosclerosis
  • cyclooxygenase inhibitor
  • 27-hydroxylase
  • ABCA1
  • foam cell

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