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mitochondrial permeability transition pore
The Mitochondrial Permeability Transition, or MPT, is defined as an increase in the permeability of the mitochondrial membranes to molecules of less than 1500 Daltons in molecular weight. MPT results from the opening of a ''mitochondrial permeability transition pore'', also known as the MPT pore or MPTP. The MPT pore is a protein pore that is formed in the inner membrane of the mitochondria under certain pathological conditions such as traumatic brain injury and stroke. Induction of the permeability transition pore can lead to mitochondrial swelling and cell death through apoptosis or necrosis depending on the particular biological setting.
==Roles in pathology==
The MPTP was originally discovered by Haworth and Hunter in 1979 and has been found to be involved in neurodegeneration, hepatotoxicity from Reye-related agents, cardiac necrosis and nervous and muscular dystrophies among other deleterious events inducing cell damage and death.〔
MPT is one of the major causes of cell death in a variety of conditions. For example, it is key in neuronal cell death in excitotoxicity, in which overactivation of glutamate receptors causes excessive calcium entry into the cell.〔 〕〔 〕〔 〕 MPT also appears to play a key role in damage caused by ischemia, as occurs in a heart attack and stroke.〔〕 However, research has shown that the MPT pore remains closed during ischemia, but opens once the tissues are reperfused with blood after the ischemic period,〔〕 playing a role in reperfusion injury.
MPT is also thought to underlie the cell death induced by Reye's syndrome, since chemicals that can cause the syndrome, like salicylate and valproate, cause MPT.〔〕 MPT may also play a role in mitochondrial autophagy.〔 Cells exposed to toxic amounts of Ca2+ ionophores also undergo MPT and death by necrosis.〔
抄文引用元・出典: フリー百科事典『 ウィキペディア（Wikipedia）』
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