Heart tissue is remarkably sensitive to oxygen deprivation. Although heart cells, like those of most tissues, rapidly adapt to anoxic conditions, relatively short periods of ischaemia and subsequent reperfusion lead to extensive tissue death during cardiac infarction. Heart tissue is not readily regenerated, and permanent heart damage is the result. Although mitochondria maintain normal heart function by providing virtually all of the heart's ATP, they are also implicated in the development of ischaemic damage. While mitochondria do provide some mechanisms that protect against ischaemic damage (such as an endogenous inhibitor of the F1Fo-ATPase and antioxidant enzymes), they also possess a range of elements that exacerbate it, including ROS (reactive oxygen species) generators, the mitochondrial permeability transition pore, and their ability to release apoptotic factors. This review considers the process of ischaemic damage from a mitochondrial viewpoint. It considers ischaemic changes in the inner membrane complexes I–V, and how this might affect formation of ROS and high-energy phosphate production/degradation. We discuss the contribution of various mitochondrial cation channels to ionic imbalances which seem to be a major cause of reperfusion injury. The different roles of the H+, Ca2+ and the various K+ channel transporters are considered, particularly the K+ATP (ATP-dependent K+) channels. A possible role for the mitochondrial permeability transition pore in ischaemic damage is assessed. Finally, we summarize the metabolic and pharmacological interventions that have been used to alleviate the effects of ischaemic injury, highlighting the value of these or related interventions in possible therapeutics.
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Review Article|
August 23 2005
Biochemical dysfunction in heart mitochondria exposed to ischaemia and reperfusion
Giancarlo Solaini;
Giancarlo Solaini
1
*Scuola Superiore di Studi Universitari e di Perfezionamento S. Anna, Classe Accademica di Scienze Sperimentali, Piazza dei Martiri della Libertà 33, 56127 Pisa, Italy
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David A. Harris
David A. Harris
2
†Department of Biochemistry, University of Oxford, South Parks Rd., Oxford OX1 3QU, U.K.
2To whom correspondence should be addressed (email harrisda@bioch.ox.ac.uk).
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Publisher: Portland Press Ltd
Received:
December 06 2004
Revision Received:
April 05 2005
Accepted:
April 25 2005
Online ISSN: 1470-8728
Print ISSN: 0264-6021
The Biochemical Society, London
2005
Biochem J (2005) 390 (2): 377–394.
Article history
Received:
December 06 2004
Revision Received:
April 05 2005
Accepted:
April 25 2005
Citation
Giancarlo Solaini, David A. Harris; Biochemical dysfunction in heart mitochondria exposed to ischaemia and reperfusion. Biochem J 1 September 2005; 390 (2): 377–394. doi: https://doi.org/10.1042/BJ20042006
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