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Review
. 1996 Apr;28(2):131-8.
doi: 10.1007/BF02110643.

The permeability transition pore as a mitochondrial calcium release channel: a critical appraisal

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Review

The permeability transition pore as a mitochondrial calcium release channel: a critical appraisal

P Bernardi et al. J Bioenerg Biomembr. 1996 Apr.

Abstract

Mitochondria from a variety of sources possess an inner membrane channel, the permeability transition pore. The pore is a voltage-dependent channel, activated by matrix Ca2+ and inhibited by matrix H+, which can be blocked by cyclosporin A, presumably after binding to mitochondrial cyclophilin. The physiological function of the permeability transition pore remains unknown. Here we evaluate its potential role as a fast Ca2+ release channel involved in mitochondrial and cellular Ca2+ homeostasis. We (i) discuss the theoretical and experimental reasons why mitochondria need a fast, inducible Ca2+ release channel; (ii) analyze the striking analogies between the mitochondrial permeability transition pore and the sarcoplasmic reticulum ryanodine receptor-Ca2+ release channel; (iii) argue that the permeability transition pore can act as a selective release channel for Ca2+ despite its apparent lack of selectivity for the transported species in vitro; and (iv) discuss the importance of mitochondria in cellular Ca2+ homeostasis, and how disruption of this function could impinge upon cell viability, particularly under conditions of oxidative stress.

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References

    1. Toxicol Lett. 1993 Apr;67(1-3):119-27 - PubMed
    1. Biophys J. 1994 Apr;66(4):942-52 - PubMed
    1. Cell Calcium. 1994 Feb;15(2):143-52 - PubMed
    1. Nature. 1993 Nov 11;366(6451):109-10 - PubMed
    1. J Biol Chem. 1995 Jan 13;270(2):672-8 - PubMed

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