Abstract
The matrix metalloproteinases/tissue inhibitors of metalloproteinases system is involved in the regulation of extracellular matrix metabolism, which plays a crucial role with regards to maintenance of tissue integrity. During the occurrence of vascular pathologies including hypertension, the balance between proteases and their inhibitors is temporally destroyed. Even though there are conflicting data in the literature regarding the expression pattern of the vascular matrix metalloproteinase system, the occurring extracellular matrix turnover leads to the change of arterial mechanical properties. For example, hypertension plays crucial role in the formation of cardiovascular remodeling which seems to be characterized by an increase in extracellular matrix. Changes in arterial stiffness, a predictor for cardiovascular morbidity and mortality, are determined by alterations in vascular extracellular matrix due to hemodynamic, genetic, or other factors. It has become increasingly evident that blockade of the renin-angiotensin-aldosterone system and other pharmacological strategies, seem to be particularly effective in reducing vascular stiffness and collagen content in human and animal models. However, the relationship between extracellular matrix metabolism and the effects of therapy in hypertensive patients needs to be further explored in larger trials over a longer period of time.
Keywords: Arterial stiffness, hypertension, matrix metalloproteinases, remodeling, therapy, extracellular matrix metabolism, tissue inhibitors, tissue integrity, vascular pathologies, hypertension, cardiovascular morbidity, arterial stiffness, renin-angiotensin-aldosterone system, hypertensive patients
Current Topics in Medicinal Chemistry
Title:The Role of Matrix Metalloproteinases in Essential Hypertension
Volume: 12 Issue: 10
Author(s): Emmanuel Androulakis, Dimitris Tousoulis, Nikolaos Papageorgiou, George Latsios, Gerasimos Siasos and Christodoulos Stefanadis
Affiliation:
Keywords: Arterial stiffness, hypertension, matrix metalloproteinases, remodeling, therapy, extracellular matrix metabolism, tissue inhibitors, tissue integrity, vascular pathologies, hypertension, cardiovascular morbidity, arterial stiffness, renin-angiotensin-aldosterone system, hypertensive patients
Abstract: The matrix metalloproteinases/tissue inhibitors of metalloproteinases system is involved in the regulation of extracellular matrix metabolism, which plays a crucial role with regards to maintenance of tissue integrity. During the occurrence of vascular pathologies including hypertension, the balance between proteases and their inhibitors is temporally destroyed. Even though there are conflicting data in the literature regarding the expression pattern of the vascular matrix metalloproteinase system, the occurring extracellular matrix turnover leads to the change of arterial mechanical properties. For example, hypertension plays crucial role in the formation of cardiovascular remodeling which seems to be characterized by an increase in extracellular matrix. Changes in arterial stiffness, a predictor for cardiovascular morbidity and mortality, are determined by alterations in vascular extracellular matrix due to hemodynamic, genetic, or other factors. It has become increasingly evident that blockade of the renin-angiotensin-aldosterone system and other pharmacological strategies, seem to be particularly effective in reducing vascular stiffness and collagen content in human and animal models. However, the relationship between extracellular matrix metabolism and the effects of therapy in hypertensive patients needs to be further explored in larger trials over a longer period of time.
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Cite this article as:
Androulakis Emmanuel, Tousoulis Dimitris, Papageorgiou Nikolaos, Latsios George, Siasos Gerasimos and Stefanadis Christodoulos, The Role of Matrix Metalloproteinases in Essential Hypertension, Current Topics in Medicinal Chemistry 2012; 12 (10) . https://dx.doi.org/10.2174/1568026611208011149
DOI https://dx.doi.org/10.2174/1568026611208011149 |
Print ISSN 1568-0266 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4294 |
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