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Mitochondrial Redox Control of Matrix Metalloproteinase Signaling in Resistance Arteries

Mitochondrial Redox Control of Matrix Metalloproteinase Signaling in Resistance Arteries Editorial Mitochondrial Redox Control of Matrix Metalloproteinase Signaling in Resistance Arteries Rhian M. Touyz he importance of free radicals in the regulation of vascular tone but also as important mediators of vascular vascular tone was recognized in the late 1980s, when growth, inflammation, and fibrosis. Tendothelium-derived relaxing factor was identified to be Cellular mechanisms whereby ROS mediate their pleiotro- 1,2 NO. More recently, it has become clear that other free radicals, pic vascular effects are complex. Multiple signaling pathways such as superoxide (O ), hydrogen peroxide (H O ), and per- 2 2 2 stimulated by myriad vasoactive agents, such as angiotensin 3,4 oxynitrite (ONOO-) also modulate vascular reactivity. How- II (Ang II), endothelin-1, and aldosterone, and numerous ever, the exact role of reactive oxygen species (ROS) in the redox-sensitive signaling molecules, including mitogen-acti- regulation of vascular contraction and relaxation remains elusive vated protein kinases, tyrosine kinases, protein tyrosine phos- because vascular effects of free radicals are heterogeneous. phatases, matrix metalloproteinases (MMPs), and transcrip- Responses may differ depending on the species studied, the 21–24 tion factors, have been implicated. vascular bed under investigation, whether the endothelium is In the present issue of Arteriosclerosis, Thombosis, and intact or denuded, and http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Arteriosclerosis, Thrombosis, and Vascular Biology Wolters Kluwer Health

Mitochondrial Redox Control of Matrix Metalloproteinase Signaling in Resistance Arteries

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ISSN
1079-5642
eISSN
1524-4636
DOI
10.1161/01.ATV.0000216428.90962.60
pmid
16556862
Publisher site
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Abstract

Editorial Mitochondrial Redox Control of Matrix Metalloproteinase Signaling in Resistance Arteries Rhian M. Touyz he importance of free radicals in the regulation of vascular tone but also as important mediators of vascular vascular tone was recognized in the late 1980s, when growth, inflammation, and fibrosis. Tendothelium-derived relaxing factor was identified to be Cellular mechanisms whereby ROS mediate their pleiotro- 1,2 NO. More recently, it has become clear that other free radicals, pic vascular effects are complex. Multiple signaling pathways such as superoxide (O ), hydrogen peroxide (H O ), and per- 2 2 2 stimulated by myriad vasoactive agents, such as angiotensin 3,4 oxynitrite (ONOO-) also modulate vascular reactivity. How- II (Ang II), endothelin-1, and aldosterone, and numerous ever, the exact role of reactive oxygen species (ROS) in the redox-sensitive signaling molecules, including mitogen-acti- regulation of vascular contraction and relaxation remains elusive vated protein kinases, tyrosine kinases, protein tyrosine phos- because vascular effects of free radicals are heterogeneous. phatases, matrix metalloproteinases (MMPs), and transcrip- Responses may differ depending on the species studied, the 21–24 tion factors, have been implicated. vascular bed under investigation, whether the endothelium is In the present issue of Arteriosclerosis, Thombosis, and intact or denuded, and

Journal

Arteriosclerosis, Thrombosis, and Vascular Biology – Wolters Kluwer Health

Published: Apr 1, 2006

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