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The Role of Mitochondria in Necrosis Following Myocardial Ischemia-Reperfusion

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Mitochondria

Part of the book series: Advances in Biochemistry in Health and Disease ((ABHD,volume 2))

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Abstract

Using the recently adopted nomenclature of cell death (Levin et al. 1999), necrosis refers to cell death and disintegration, regardless of the pathway; the modifiers apoptotic and oncotic are used to refer to the mechanism of death. Traditionally cell death following ischemia has been thought to be primarily oncotic necrosis. As detailed in numerous reviews, during ischemia when the ATP falls to very low levels, the ion pumps cannot function resulting in a rise in Ca2+ which further consumes ATP (Farber and Gerson 1984; Jennings et al. 1990; Jennings and Reimer 1981; Jennings and Steenbergen 1985). The rise in Ca2+ during ischemia and reperfusion leads to mitochondrial Ca2+ accumulation, particularly during reperfusion when oxygen is reintroduced. Reintroduction of oxygen provides a terminal electron acceptor (oxygen) allowing electron transport to occur; however damage to electron transport chain can lead to increased mitochondrial generation of reactive oxygen species (ROS).

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Authors
  1. Elizabeth Murphy
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  2. Charles Steenbergen
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Editor information

Editors and Affiliations

  1. Department of Pharmacology, University of South Alabama, Mobile, AL, 36688-0001, USA

    Stephen W. Schaffer

  2. Bristol Royal Infirmary, Bristol, BS2 8HW, UK

    M-Saadeh Suleiman

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Murphy, E., Steenbergen, C. (2007). The Role of Mitochondria in Necrosis Following Myocardial Ischemia-Reperfusion. In: Schaffer, S.W., Suleiman, MS. (eds) Mitochondria. Advances in Biochemistry in Health and Disease, vol 2. Springer, New York, NY. https://doi.org/10.1007/978-0-387-69945-5_13

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