This Article Free upon publication Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Liang, C.-P. Articles by Tall, A. R. Search for Related Content PubMed PubMed Citation Articles by Liang, C.-P. Articles by Tall, A. R.

(Circulation Research. 2007;100:1546.)
© 2007 American Heart Association, Inc.

Reviews

The Macrophage at the Crossroads of Insulin Resistance and Atherosclerosis

Chien-Ping Liang, Seongah Han, Takafumi Senokuchi, Alan R. Tall

From the Division of Molecular Medicine, Department of Medicine, Columbia University, New York.

Correspondence to Chien-Ping Liang, Division of Molecular Medicine, Department of Medicine, Columbia University, 630 West 168th St., New York, NY 10032. E-mail CL534{at}columbia.edu

This Review is part of a thematic series on the Atherosclerosis in Diabetes: Dyslipidemia vs Hyperglycemia, which includes the following articles:

Do Glucose and Lipids Exert Independent Effects on Atherosclerotic Lesion Initiation or Progression to Advanced Plaques?

Recipes for Creating Animal Models of Diabetic Cardiovascular Disease

The Macrophage at the Crossroads of Insulin Resistance and Atherosclerosis

Lipids, glucose, and oxidative reactions in diabetes and atherosclerosis
Karin E. Bornfeldt Guest Editor

The macrophage has emerged as an important player in the pathogenesis of both atherosclerosis and insulin resistance. Cross-talk between inflammatory macrophages and adipocytes may be involved in insulin resistance in peripheral tissues. Defective insulin signaling in cells of the arterial wall including macrophages may promote the development of atherosclerosis. Insulin resistant macrophages are more susceptible to endoplasmic reticulum stress and apoptosis in response to various stimuli such as nutrient deprivation, free cholesterol loading, and oxidized LDL. Increased apoptosis of insulin resistant macrophages and impaired phagocytic clearance of apoptotic cells by insulin resistant macrophages in atherosclerotic lesions may lead to enhanced postapoptotic necrosis, larger lipid-rich cores, increased inflammation, and more complex vulnerable plaques.

Key Words: atherosclerosis • insulin resistance • diabetes mellitus • macrophages • apoptosis

This article has been cited by other articles:

				E. Herczenik and M. F. B. G. Gebbink Molecular and cellular aspects of protein misfolding and disease FASEB J, July 1, 2008; 22(7): 2115 - 2133. [Abstract] [Full Text] [PDF]

				M. Minami, K. Shimizu, Y. Okamoto, E. Folco, M.-L. Ilasaca, M. W. Feinberg, M. Aikawa, and P. Libby Prostaglandin E Receptor Type 4-associated Protein Interacts Directly with NF-{kappa}B1 and Attenuates Macrophage Activation J. Biol. Chem., April 11, 2008; 283(15): 9692 - 9703. [Abstract] [Full Text] [PDF]

				J. W. Han, K. Shimada, W. Ma-Krupa, T. L. Johnson, R. M. Nerem, J. J. Goronzy, and C. M. Weyand Vessel Wall-Embedded Dendritic Cells Induce T-Cell Autoreactivity and Initiate Vascular Inflammation Circ. Res., March 14, 2008; 102(5): 546 - 553. [Abstract] [Full Text] [PDF]