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Cardiovascular Research Advance Access originally published online on August 9, 2008
Cardiovascular Research 2008 80(1):1-2; doi:10.1093/cvr/cvn214
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org

Adenine nucleotide translocator, a mitochondrial carrier protein, and fate of cardiomyocytes after ischaemia/reperfusion

Masaya Tanno* and Tetsuji Miura

Second Department of Internal Medicine, Sapporo Medical University, S1 W16, Chuo-ku, Sapporo, 060-8556, Japan

* Corresponding author. Tel: +81 11 611 2111; fax: +81 11 644 7958. E-mail address: tannom@sapmed.ac.jp

This editorial refers to ‘Phosphoproteome analysis of isoflurane-protected heart mitochondria: phosphorylation of adenine nucleotide translocator-1 on Tyr194 regulates mitochondrial function’ by Feng et al.,11 pp. 20–29, this issue.

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Mitochondria have multiple roles in the development of ischaemia/reperfusion injury. Consumption of ATP by mitochondrial ATPase during ischaemia and generation of reactive oxygen species (ROS) from complex III during ischaemia/reperfusion are detrimental to cardiomyocytes, whereas uptake of cytosolic Ca2+ into mitochondria attenuates cytosolic Ca2+ overload and thus activation of Ca2+-activated proteases such as calpain. However, the most important event in the mitochondria of cardiomyocytes subjected to ischaemia/reperfusion is opening of the mitochondrial permeability transition pore (mPTP).1 Although its molecular structure is still controversial, mPTP apparently consists of an adenine nucleotide translocator (ANT) in the inner membrane, . . . [Full Text of this Article]


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