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Cardiovascular Research 2002 55(1):13-15; doi:10.1016/S0008-6363(02)00443-1
© 2002 by European Society of Cardiology
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Copyright © 2002, European Society of Cardiology

Mast cells feel the strain

Adrian H Chester*

Department of Cardiothoracic Surgery, National Heart and Lung Institute, Imperial College of Science Technology and Medicine, Heart Science Centre, Harefield Hospital, Harefield, Middlesex UB9 6JH, UK

* Tel.: +44-1895-828-727; fax: +44-1895-828-900 a.chester@ic.ac.uk

Received 16 April 2002; accepted 17 April 2002

The first 10% of the full text of this article appears below.

See article by Huang et al. [1] (pages 150–160) in this issue.

Mast cells are implicated to be involved in the pathogenesis of atherosclerosis and acute coronary syndromes. However, the contribution of mast cells in the initiation of atherogenic mechanisms, and the role of mediators they release is not fully understood. In this issue of Cardiovascular Research, Huang et al. [1] provide evidence that mast cells can contribute to stress related cardiac disease. They showed that mast cells become activated in response to acute restraint stress in mice. This effect was enhanced in ApoE knock-out mice. These mice were seen to have higher levels of histamine and a greater number of mast cells, compared to wild type. The findings provide important evidence that acute coronary syndromes can be mediated by neuroinflammatory reactions.

Mast cells . . . [Full Text of this Article]


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M. Huang, X. Pang, K. Karalis, and T. C. Theoharides
Stress-induced interleukin-6 release in mice is mast cell-dependent and more pronounced in Apolipoprotein E knockout mice
Cardiovasc Res, July 1, 2003; 59(1): 241 - 249.
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