Cyclophilin D is a component of mitochondrial permeability transition and mediates neuronal cell death after focal cerebral ischemia.

By Anna C. Schinzel, O. Takeuchi, Zhihong Huang, J. Fisher, Zhipeng Zhou, Jeffery Rubens, C. Hetz, N. Danial, M. Moskowitz, S. Korsmeyer. Proceedings of the National Academy of Sciences of the United States of America, 2005

838 citations recorded by the source corpus.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/940da9e6871a4805aec119a319d00bd7560fa443

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Citations in the corpus

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).”
Cell Death Signaling. (2015, background): “2005) and display diminished tissue damage under conditions of I/R (Baines et al. 2005; Nakagawa et al. 2005; Schinzel et al. 2005).”
Voltage-dependent anion channels are dispensable for mitochondrial-dependent cell death (2007, background): “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).”
Cell Biology of Ischemia/Reperfusion Injury (2012, background): “These pharmacological data have since been confirmed by the generation of CypD-deficient mice, which exhibit an innate protection against cardiac, hepatic, and renal I/R injury (Baines et al., 2005; Devalaraja-Narashimha et al., 2009; Schinzel et al., 2005).”
Cell death by necrosis: towards a molecular definition. (2007, background): “In addition, CypD-deficient mice are resistant tocardiac injury by ischemia‐reperfusion [40,41] and focal cerebral ischemia [ 42 ].”
Neuronal Cell Death. (2018, neutral): “Mitochondria from cyclophilin D-knockout mice have been shown to exhibit resistance to calcium-induced mPTP, and these mice were more resistant to ischemia-induced brain cell death than their counterparts expressing cyclophilin D, suggesting an essential role of mPTP in ischemic brain injury (602).”
Pathophysiology of Acute Kidney Injury (2012, neutral): “Neurons from cyclophilin D knockout mice, have a reduced level of MPT in response to oxidant stress when compared to neurons from wild type animals (478).”
Early deficits in synaptic mitochondria in an Alzheimer's disease mouse model (2010, background): “Recent studies provide substantial evidence that genetic deficiency of CypD protects cells from Ca- and oxidative stress-induced cell death (29, 45).”
The changing faces of glutathione, a cellular protagonist. (2003, background): “In contrast, the prolyl isomerase cyclophilin D in the mitochondrial matrix is an essential regulator of MPT and the only genetically proven indispensable MPT component (Baines et al., 2005; Basso et al., 2005; Nakagawa et al., 2005; Schinzel et al., 2005).”
Superoxide Flashes in Single Mitochondria (2008, neutral): “Given significant limitations inherent in pharmacological manipulation of mPTP activity, we also determined the effect of RNA interference (siRNA) knockdown of cyclophilin D, a critical component of the mPTP (Baines et al., 2005; Basso et al., 2005; Nakagawa et al., 2005; Schinzel et al., 2005 ).”
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].”