The Pathophysiology of Mitochondrial Cell Death

By Douglas R. Green, Guido Kroemer. Science, 2004

3,508 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/0edfeb6c54dce7e3542043ffdc0a7ea39e0be46d

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Citations in the corpus

Mitochondrial biology and oxidative stress in Parkinson disease pathogenesis (2008, neutral): “(2006)42 Greene et al. (2003)43 Pesah et al.”
Chronic lymphocytic leukemia requires BCL2 to sequester prodeath BIM, explaining sensitivity to BCL2 antagonist ABT-737. (2007, background): “Mitochondrial outer membrane permeabilization (MOMP) follows BAX and BAK oligomerization, allowing release of cytochrome c and other proapoptotic factors into the cytosol (10, 11).”
Caspase-independent cell death (2005, background): “In this case, caspase activation constitutes a sign rather than a mechanism of cell death, and the decisive event has occurred upstream or at the level of MOMP, which frequently marks the 'point of no return' of the lethal proces”
Lysosomes and autophagy in cell death control (2005, background): “Although resistance to cell death is attributed to the inhibition of classic apoptosis and its hallmarks — particularly CASPASE activation and MITOCHONDRIAL OUTER-MEMBRANE PERMEABILIZATION (MOMP”
Elucidating mechanisms of drug-induced toxicity (2005, background): “and the mitochondrial permeability transition (a barrier to prevent loss of components of the organelle), which allows release of cytochrome c and initiates apoptosis in response to chemical stressor”
Intrinsic tumour suppression (2004, background): “The ‘intrinsic’ pathway is the primary death programme responsive to the signals of survival factors, cell stress and injur”
Mitochondrial creatine kinase in human health and disease. (2006, neutral): “The latter may trigger apoptosis by the release of proapoptotic proteins like cytochrome c or lead to necrotic cell death due to energy depletion [69,74,95].”
Life in the balance: how BH3-only proteins induce apoptosis. (2005, background): “The resulting membrane permeabilization releases pro-apoptotic proteins, such as cytochrome c, that provoke activation of the caspases mediating cell demolition [5].”
Glutaminolysis and Transferrin Regulate Ferroptosis (2015, background): “In multicellular organisms, programmed cell death, particularly apoptosis, is frequently activated in a highly orchestrated manner to fulfill specific physiological functions (Budihardjo et al., 1999; Danial and Korsmeyer, 2004; Fuchs and Steller, 2011; Green and Kroemer, 2004; Thompson, 1995).”
Cytochrome c acts as a cardiolipin oxygenase required for release of proapoptotic factors (2005, background): “In vertebrate cells, the most common form of apoptosis proceeds through the mitochondrial (intrinsic) death pathwa”
Reactive Oxygen Species in Inflammation and Tissue Injury (2014, neutral): “This whole complex is collectively known as ‘‘apoptosome’’ (151) (Fig.”
Malignant astrocytic glioma: genetics, biology, and paths to treatment. (2007, background): “…classical anti-apoptotic Bcl-2 family members (BAK, BAD, BID, BAX, BCL-X L , MCL-1) modulate apoptosis signaling by preserving mitochondrial membrane integrity and the release of cytochrome c, which effects the caspase cascade and the apoptotic program (for review, see Green and Kroemer 2004).”
Curcumin: Preventive and Therapeutic Properties in Laboratory Studies and Clinical Trials (2008, neutral): “It is known that members of the bcl-2 family are involved in mitochondrial membrane permeability (93), and therefore their downregulation may contribute, to some extent, to the increased mitochondrial permeability, edema, induction of apoptosis, and cell death observed in vitro (241).”
The role of mitochondria in apoptosis. (2008, background): “Recent studies have uncovered that mitochondria are the garden of cell death that plays a crucial role in regulating cell death pathways (17, 18).”
Plant mitochondrial pathway leading to programmed cell death (2007, background): “…the intrinsic pathway is evolutionarily conserved in multicellular organisms and is characterised by signal sensing and amplification by mitochondria, mediated by the release of the mitochondrial apoptogenic factors (Desagher and Martinou 2000, Green and Kroemer 2004, Kroemer and Reed 2000).”