Cardiovascular Research Advance Access originally published online on August 6, 2008
Cardiovascular Research 2008 80(1):5-6; doi:10.1093/cvr/cvn212
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org
High-mobility group box 1 protein (HMGB1) in ischaemic heart disease: beneficial or deleterious?
Department of Cardiovascular Medicine, Shinshu University Graduate School of Medicine, 3-1-1 Asahi, Matsumoto, Nagano 390-8621, Japan
Corresponding author. Tel: +81 263 37 3352; fax: +81 263 37 2573. E-mail address: masafumi@shinshu-u.ac.jp
This editorial refers to High-mobility group box 1 restores cardiac function after myocardial infarction in transgenic mice by Kitahara et al.,4 pp. 40–46, this issue.
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High-mobility group box 1 (HMGB1; also known as amphoterin) protein was identified more than 30 years ago as a non-chromosomal nuclear protein that maintains the nucleosome structure and regulates gene transcription.1 HMGB1 is highly conserved among species, has over 98% identity among all mammals, and is ubiquitously expressed in almost all types of cells. HMGB1-deficient mice are viable but die shortly after birth due to hypoglycaemia, suggesting that its nuclear functions are essential for survival. In 1999, Wang et al.2 discovered that HMGB1 functions as a delayed mediator in inflammatory responses in sepsis and showed that the inhibition of HMGB1 confers significant protection against the lethal effects of endotoxin, indicating the importance of
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Cardiovasc Res 2008 80: 40-46.
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T. Kohno, T. Anzai, K. Naito, T. Miyasho, M. Okamoto, H. Yokota, S. Yamada, Y. Maekawa, T. Takahashi, T. Yoshikawa, et al. Role of high-mobility group box 1 protein in post-infarction healing process and left ventricular remodelling Cardiovasc Res, February 15, 2009; 81(3): 565 - 573. [Abstract] [Full Text] [PDF] |
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