Abstract
The cellular role of mitochondria includes ATP generation and the modulation of cytosolic calcium signals, besides being the “crossroads” for several cell death pathways. The maintenance of optimal mitochondrial functioning during the disease process increases the chances for survival. For example, ischaemia followed by reperfusion is known to negatively affect mitochondrial function, namely by inducing a deleterious condition called mitochondrial permeability transition (MPT). The MPT is responsible for mitochondrial dysfunction and can ultimately lead to cell death. Therefore, it seems important to protect mitochondrial function in cardiac disease. Carvedilol, a β-adrenergic receptor antagonist with antioxidant properties, has a positive impact on cardiac mitochondria during in vitro, ex-vivo and in vivo models of cardiac dysfunction. Particularly, carvedilol was shown to inhibit MPT in isolated heart mitochondria and protect mitochondria against the oxidative damage induced by the xanthine oxidase / hypoxanthine pro-oxidant system. The observation that carvedilol acts as an inhibitor of mitochondrial complex-I is also of importance, since this mitochondrial system was proposed as cause of the cardiotoxicity associated with the antineoplasic drug doxorubicin. This review points out the major findings concerning the positive impact of carvedilol on mitochondrial function and its use in the treatment of myocardial diseases where oxidative stress is known to be involved.
Keywords: mitochondria, carvedilol, myocyte
Current Vascular Pharmacology
Title: Are the Antioxidant Properties of Carvedilol Important for the Protection of Cardiac Mitochondria?
Volume: 3 Issue: 2
Author(s): Paulo J. Oliveira, Lino Goncalves, Pedro Monteiro, Luis A. Providencia and Antonio J. Moreno
Affiliation:
Keywords: mitochondria, carvedilol, myocyte
Abstract: The cellular role of mitochondria includes ATP generation and the modulation of cytosolic calcium signals, besides being the “crossroads” for several cell death pathways. The maintenance of optimal mitochondrial functioning during the disease process increases the chances for survival. For example, ischaemia followed by reperfusion is known to negatively affect mitochondrial function, namely by inducing a deleterious condition called mitochondrial permeability transition (MPT). The MPT is responsible for mitochondrial dysfunction and can ultimately lead to cell death. Therefore, it seems important to protect mitochondrial function in cardiac disease. Carvedilol, a β-adrenergic receptor antagonist with antioxidant properties, has a positive impact on cardiac mitochondria during in vitro, ex-vivo and in vivo models of cardiac dysfunction. Particularly, carvedilol was shown to inhibit MPT in isolated heart mitochondria and protect mitochondria against the oxidative damage induced by the xanthine oxidase / hypoxanthine pro-oxidant system. The observation that carvedilol acts as an inhibitor of mitochondrial complex-I is also of importance, since this mitochondrial system was proposed as cause of the cardiotoxicity associated with the antineoplasic drug doxorubicin. This review points out the major findings concerning the positive impact of carvedilol on mitochondrial function and its use in the treatment of myocardial diseases where oxidative stress is known to be involved.
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Cite this article as:
Oliveira J. Paulo, Goncalves Lino, Monteiro Pedro, Providencia A. Luis and Moreno J. Antonio, Are the Antioxidant Properties of Carvedilol Important for the Protection of Cardiac Mitochondria?, Current Vascular Pharmacology 2005; 3 (2) . https://dx.doi.org/10.2174/1570161053586903
DOI https://dx.doi.org/10.2174/1570161053586903 |
Print ISSN 1570-1611 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-6212 |
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Cardiovascular disease still remains the leading cause of death in Chronic and End Stage Kidney Disease, accounting for more than half of all deaths in dialysis patients. During the past decade, research has been focused on novel therapeutic agents that might delay or even reverse cardiovascular disease and vascular calcification, ...read more
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