The path from mitochondrial ROS to aging runs through the mitochondrial permeability transition pore
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The path from mitochondrial ROS to aging runs through the mitochondrial permeability transition pore
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...
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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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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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Mitochondrial ATP generation by oxidative phosphorylation combines the stepwise oxidation by the electron transport chain (ETC) of the reducing equivalents NADH and FADH2 with the generation of ATP by the ATP synthase. Recent studies show that the ATP synthase is not only essential for the generation of ATP but may also contribute to the formation of the mitochondrial permeability transition po...
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Mitochondrial permeability transition pore (MPTP) is a transient structure formed in the inner mitochondrial membrane (IMM) upon oxidative challenge of the organelle. The transition is a Ca 2+ -dependent increase of permeability of IMM leading to loss of transmembrane potential (∆ψm), mitochondrial swelling and, finally, rupture of outer mitochondrial membrane leading to release of factors caus...
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ژورنال
عنوان ژورنال: Aging Cell
سال: 2017
ISSN: 1474-9718
DOI: 10.1111/acel.12650