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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2009.1
- 수록면
- 1,007 - 1,019 (13page)
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초록· 키워드
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Opening of mitochondrial permeability transition pore (mPTP) was found to have a critical role
in cell death from ischemia/reperfusion (I/R) injury experimentally in the late 1980’s.
Thereafter, tremendous efforts have been made to define the molecular composition of mPTP and
underlying mechanisms of its opening. mPTP opening, so far, has been demonstrated with the
conformational changes of the mitochondrial protein components including cyclophilin-D, adenine
nucleotide translocase, and voltage-dependent anion channel, which were induced by the
modification of the levels of Ca2+, phosphate, mitochondrial membrane potential, intracellular pH
and adenine nucleotide. At present, genetic modulation of the expression of protein components
are being used in the investigation of its properties, presenting novel mechanisms of mPTP
opening, including phosphate carrier. For therapeutic intervention, cyclosporin A and its analogues
were first to be demonstrated to inhibit the opening of mPTP, affecting cyclophilin-D. There are
numerous pharmacological substances that have direct or indirect effects on mPTP opening,
including bongkrekic acid, reactive oxygen species scavengers, calcium channel blockers, and
Na+/H+ exchanger-1 inhibitors, but only cyclosporin A was clinically tried to limit the myocardial
infarction. Conditioning interventions, ischemic or anesthetic, have also been shown to be effective
in limiting the detrimental effects of I/R injury. These interventions are commonly related to specific
receptors on cell membrane and then signal transduction pathway consisting of many protein
kinases, which eventually lead to mitochondria. And being presented are experimental evidences
that inhibition of mPTP opening is a primary mechanism of these conditioning interventions. In
conclusion, mPTP opening is now presented as primary mechanism and therapeutic target of I/R
injury, but precise mechanism and standardized treatment method are needed to be clarified.
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