Mitochondrial membrane permeabilization in cell death.

By Guido Kroemer, L. Galluzzi, C. Brenner. Physiological Reviews, 2007

3,637 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/9fbc5c35253c11ca2ae7744b520bb77c1c496c38

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Citations in the corpus

Self-eating and self-killing: crosstalk between autophagy and apoptosis (2007, background): “Thus, the absence of redox equivalents may favour oxidative reactions that trigger apoptosis, presumably through a direct effect on mitochondria, and the absence of NADPH 2 and ATP may de-inhibit the activation of caspase-2 or MOM”
Mitotic catastrophe: a mechanism for avoiding genomic instability (2011, background): “Whereas apoptosis was long ago recognized as a programmed mechanism manifesting with specific morphological and biochemical markers, including cytoplasmic shrinkage (that is, pyknosis) and chromatin condensatio”
Calcium and apoptosis: ER-mitochondria Ca2+ transfer in the control of apoptosis (2008, background): “At the same time, mitochondria are important checkpoints of the apoptotic process, as they may release caspase cofactors (Kroemer et al., 2007).”
Life and death in peripheral T cells (2007, background): “This pathway crucially depends on permeabilization of the outer mitochondrial membran”
Autophagy and aging. (2011, background): “Mitochondrial membrane permeabilization (MMP) is (one of) the rate-limiting steps of cell death, and the threshold beyond which MMP affecting a variable portion of mitochondria kills cells is likewise determined by the autophagic removal of permeabilized organelles (Kroemer et al., 2007).”
Consensus guidelines for the detection of immunogenic cell death (2014, background): “239241 The externalization of phosphatidylserine (a phospholipid normally restricted to the inner leaflet of the plasma membrane) indeed accompanies multiple (though not all) instances of apoptotic cell death,(16,242-245) while the permanent dissipation of the Dcm as a result of mitochondrial outer ”
Cell Biology of Ischemia/Reperfusion Injury (2012, background): “Caspase-3 acts as the cell’s executioner by proteolyzing many cellular proteins (Broughton et al., 2009; Kroemer et al., 2007; Whelan et al., 2010).”
Metabolic Modulation of Glioblastoma with Dichloroacetate (2010, background): “Although controversial [reviewed in (14)], the efflux of proapoptotic mediators through the mitochondrial transition pore (MTP) depends in part on mitochondrial membrane potential (DYm), and thus, mitochondrial hyperpolarization may mark an apoptosis resistance state (3, 15).”
Targeting mitochondria for cancer therapy (2010, background): “Multiple apoptosis-inducing and necrosis-inducing biochemical cascades converge on mitochondria to cause their deregulation and permeabilizatio”
Decoding cell death signals in liver inflammation. (2013, background): “In response to multiple stimuli, however, ROS levels exceed the buffer capacity of these systems, resulting first in the activation of an adaptive response aimed at the re-establishment of redox homeostasis coupled to an inflammatory response [53], and then in intracellular damage, progressive mitoc”
p53 opens the mitochondrial permeability transition pore to trigger necrosis (2012, methodology): “To look for evidence of p53-induced functional alterations of this pore, we used the fluorescent dye calcein, a highly selective indicator of sustained PTP opening in situ (Kroemer et al., 2007).”
Mitochondrial fusion, fission and autophagy as a quality control axis: the bioenergetic view. (2008, methodology): “the current review and are detailed elsewhere [15, 37-39].”