Mitochondrial control of cell death
By Guido Kroemer, John Calvin Reed. Nature Medicine, 2000
3,233 citations recorded by the source corpus.
Subfields: Molecular Biology
View Paper: https://www.semanticscholar.org/paper/4e43d3a11bc51c49cf2f59435ff12e32d09a6495
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Citations in the corpus
- Inhibition of Macroautophagy Triggers Apoptosis (2005, background): “6A and B), suggesting that, as in other paradigms of apoptosis (21, 22, 38), caspase activation occurred downstream of MMP.”
- Glutathione in Cancer Biology and Therapy (2006, neutral): “acid (γ -Glu-aa) transporter; (3) dipeptidases; (4) Cyst(e)ine transporters; (5) γ -Glu-cyclotransferase; (6) 5-oxoprolinase; (7) GCS; (8) GSHS; (9) GPx; (10) GR; (11) transhydrogenases; (12) GSTs.”
- Role of hypoxia in cancer therapy by regulating the tumor microenvironment (2019, background): “Cyt c and other mitochondrial polypeptides were found to be released from the mitochondrial intermembrane space in the mitochondrial pathway [84].”
- Oxidative Stress: A Key Modulator in Neurodegenerative Diseases (2019, background): “The enzyme and protein required for the oxidative phosphorylation are encoded by the mitochondrial DNA [9,10].”
- Viruses and apoptosis (2001, background): “It has recently become evident that mitochondria play a pivotal role in both the life and death of the cell (Green & Reed 1998; Kroemer & Reed 2000).”
- Oxidative Stress and Neurodegenerative Diseases: A Review of Upstream and Downstream Antioxidant Therapeutic Options (2009, background): “Any mutation in Mt DNA leads to impaired ATP generation and perturbed oxidative phosphorylation cascade that may further lock the neuronal function [33].”
- ROS stress in cancer cells and therapeutic implications. (2004, background): “Decrease in the mitochondrial membrane potential, impairment of the mitochondrial respiratory chain, and depletion of ATP are characteristic consequences of oxidative stress (Kroemer and Reed, 2000; Brown and Borutaite, 2002).”
- The pathophysiology of acute myocardial infarction and strategies of protection beyond reperfusion: a continual challenge. (2016, background): “Apoptosis is an energy-dependent mode of cell death with typical DNA fragmentation but lack of an inflammatory response, and is initiated extrinsically through sarcolemmal receptors and intrinsically by release of cytochrome C from damaged mitochondria.(46,47) Opening of the mitochondrial permeabili”