LOX-1 The Multifunctional Receptor Underlying Cardiovascular Dysfunction
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- Ogura Sayoko
- Department of Vascular Physiology, National Cardiovascular Center
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- Kakino Akemi
- Department of Vascular Physiology, National Cardiovascular Center
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- Sato Yuko
- Department of Vascular Physiology, National Cardiovascular Center
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- Fujita Yoshiko
- Department of Vascular Physiology, National Cardiovascular Center
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- Iwamoto Shin
- Department of Vascular Physiology, National Cardiovascular Center
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- Otsui Kazunori
- Department of Vascular Physiology, National Cardiovascular Center
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- Yoshimoto Ryo
- Department of Vascular Physiology, National Cardiovascular Center
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- Sawamura Tatsuya
- Department of Vascular Physiology, National Cardiovascular Center
Bibliographic Information
- Other Title
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- The Multifunctional Receptor Underlying Cardiovascular Dysfunction
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Abstract
Oxidatively modified low-density lipoprotein (oxLDL) is implicated in the pathogenesis of atherosclerosis. Endothelial dysfunction is the initial change in the vascular wall that induces morphological changes for atheroma-formation. Lectin-like oxidized LDL receptor-1 (LOX-1) was identified as the receptor for oxLDL that was thought to be a major cause of endothelial dysfunction. LOX-1 has been demonstrated to contribute not only to endothelial dysfunction, but also to atherosclerotic-plaque formation, myocardial infarction and intimal thickening after balloon injury. Recent findings on the genetics of LOX-1 and the methodology to detect it and its ligands would further facilitate the examination of the receptor's pathophysiological contribution in atherosclerosis. Furthermore, LOX-1-related tools might open new gateways from diagnosis to therapeutics for cardiovascular diseases. (Circ J 2009; 73: 1993-1999)<br>
Journal
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- Circulation Journal
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Circulation Journal 73 (11), 1993-1999, 2009
The Japanese Circulation Society
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Details 詳細情報について
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- CRID
- 1390001205102420992
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- NII Article ID
- 10025936843
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- NII Book ID
- AA11591968
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- ISSN
- 13474820
- 13469843
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- Text Lang
- en
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- Data Source
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- JaLC
- Crossref
- CiNii Articles
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- Abstract License Flag
- Disallowed