The mitochondrial permeability transition from yeast to mammals
نویسندگان
چکیده
منابع مشابه
The mitochondrial permeability transition pore.
This chapter reviews recent advances in the identification of the structural elements of the permeability transition pore. The discovery that cyclosporin A (CsA) inhibits the pore proved instrumental. Various approaches indicate that CsA blocks the pore by binding to cyclophilin (CyP)-D. In particular, covalent labelling of CyP-D in situ by a photoactive CsA derivative has shown that pore ligan...
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Excessive production of mitochondrial reactive oxygen species (mROS) is strongly associated with mitochondrial and cellular oxidative damage, aging, and degenerative diseases. However, mROS also induces pathways of protection of mitochondria that slow aging, inhibit cell death, and increase lifespan. Recent studies show that the activation of the mitochondrial permeability transition pore (mPTP...
متن کاملMitochondrial Permeability Transition in Rat
42 Onset of the mitochondrial permeability transition (MPT) is the penultimate event 43 leading to lethal cellular ischemia/reperfusion injury, but the mechanisms precipitating 44 the MPT after reperfusion remain unclear. Here, we investigated the role of 45 mitochondrial free Ca and reactive oxygen species (ROS) in pHand MPT-dependent 46 reperfusion injury to hepatocytes. Cultured rat hepatocy...
متن کاملPostconditioning inhibits mitochondrial permeability transition.
BACKGROUND Brief periods of ischemia performed just at the time of reperfusion can reduce infarct size, a phenomenon called "postconditioning." After reflow, opening of the mitochondrial permeability transition pore (mPTP) has been involved in lethal reperfusion injury. We hypothesized that postconditioning may modulate mPTP opening. METHODS AND RESULTS Anesthetized open-chest rabbits underwe...
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Ischemia-associated oxidative damage leading to necrosis is a major cause of catastrophic tissue loss, and elucidating its signaling mechanism is therefore of paramount importance. p53 is a central stress sensor responding to multiple insults, including oxidative stress to orchestrate apoptotic and autophagic cell death. Whether p53 can also activate oxidative stress-induced necrosis is, howeve...
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ژورنال
عنوان ژورنال: FEBS Letters
سال: 2010
ISSN: 0014-5793
DOI: 10.1016/j.febslet.2010.04.023