The MPT (mitochondrial permeability transition) occurs when a protein pore opens in the mitochondrial inner membrane in response to calcium overloading, adenine nucleotide depletion and oxidative stress, causing the disruption of mitochondrial function. For a number of years, this intriguing phenomenon was thought to be an in vitro curiosity of uncertain relevance to mitochondrial function within cells and tissues. However, this view was fundamentally altered with the help of three papers published in the Biochemical Journal in the 1980s and 1990s. Together, these studies demonstrated that CsA (cyclosporin A) selectively blocked induction of the MPT, that the mitochondrial matrix protein cyclophilin D was required for induction of the MPT, and that the MPT contributed to tissue damage during IR (ischaemia–reperfusion) injury.

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