Loss of cyclophilin D reveals a critical role for mitochondrial permeability transition in cell death

By Christopher P. Baines, R. A. Kaiser, N. Purcell, N. Blair, H. Osińska, Michael A. Hambleton, E. Brunskill, M. R. Sayen, R. Gottlieb, Gerald W. Dorn II and 2 more. Nature, 2005

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Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/95db5579376e04594a275d77291dd077a6670c2f

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Citations in the corpus

Dimers of mitochondrial ATP synthase form the permeability transition pore (2013, methodology): “CyPD sensitizes the PTP to Ca 2 + , as deduced from experiments in mitochondria from Ppif − / − mice where the PT required higher loads of matrix Ca 2 + (19 – 22), a behavior that is perfectly matched by the MMC (23).”
Mitochondria take center stage in aging and neurodegeneration (2005, background): “Mice lacking cyclophilin are resistant to Ca(2) overload and oxidative stress–induced cell death as well as ischemia/ reperfusion-induced cardiac injury.(2,3) These findings argue against a role of the MPT in apoptotic cell death, although a role in another nonapoptotic cell death pathway termed nec”
Cardiotoxicity of the cancer therapeutic agent imatinib mesylate (2006, background): “This was largely inhibited by cyclosporin A, an inhibitor of cyclophilin D–mediated pore openin”
Necrosis, a well-orchestrated form of cell demise: signalling cascades, important mediators and concomitant immune response. (2006, background): “In addition, CypD-deficient mice are highly resistant to cardiac injury induced by ischemia/ reperfusion, confirming that CypD-dependent MPT regulates some forms of necrotic death [118–121].”
Response to myocardial ischemia/reperfusion injury involves Bnip3 and autophagy (2007, background): “Moreover, mice lacking cyclophilin D, a component of the MPTP, are more resistant to I/R injury, whereas transgenic mice overexpressing cyclophilin D exhibited swollen mitochondria and increased spontaneous cell death.(35) This suggests that Bnip3-mediated mitochondrial damage through opening of the”
Cell Death Signaling. (2015, background): “Ischemia/reperfusion injury (I/R), for example, causes cell death when a tissue is transiently deprived of blood supply and is then restored.”
Voltage-dependent anion channels are dispensable for mitochondrial-dependent cell death (2007, methodology): “Although recent genetic studies have confirmed a regulatory role for cyclophilin D in MPT (24,27-29), mice lacking Ant1/2 still exhibit a classical MPT response that was inhibited with cyclosporine A (30).”
Necrotic death as a cell fate. (2006, background): “In CypD-deficient cells, cytochrome c release and caspase activation occur normally following apoptotic stimuli TNF , staurosporine, etoposide, and activation of proapoptotic Bcl-2 family members Bax, Bak, and tBid (Baines et al. 2005; Basso et al. 2005; Nakagawa et al. 2005; Schinzel et al. 2005).”
Mechanisms underlying acute protection from cardiac ischemia-reperfusion injury. (2008, background): “Mice with cardiac specific loss of cyclophilin were shown to be less sensitive to calcium activation of MPT and were also shown to have significantly smaller infarcts following ischemia-reperfusion (16).”