Mitochondrial free cholesterol loading sensitizes to TNF- and Fas-mediated steatohepatitis.
By M. Marí, Francisco Caballero, A. Colell, A. Morales, J. Caballería, Anna Fernández, C. Enrich, J. Fernández-Checa, C. Garcia-Ruiz. Cell Metabolism, 2006
613 citations recorded by the source corpus.
Subfields: Cell Biology, Epidemiology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/7990d61cea3f524c6edd11c937a720bf8c769a8e
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Citations in the corpus
- Mitochondrial Glutathione, a Key Survival Antioxidant (2009, background): “In a recent study, by using genetic and nutritional models of NASH, we observed that free cholesterol accumulation in mitochondria, but not TG or FFA loading, sensitizes hepatocytes to TNF, contributing to the transition from steatosis to steatohepatitis through mGSH depletion (92).”
- Hepatic lipotoxicity and the pathogenesis of nonalcoholic steatohepatitis: The central role of nontriglyceride fatty acid metabolites (2010, background): “However, mitochondria cannot make glutathione, and studies have shown that this sensitive pool can be depleted, resulting in apoptotic cell death and steatohepatitis.(105,106) After meals, fatty acids delivered to the liver are not needed as a source of energy and are shuttled away from mitochondria”
- Evolution of inflammation in nonalcoholic fatty liver disease: The multiple parallel hits hypothesis (2010, background): “Free fatty acids and cholesterol, especially when accumulated in mitochondria, are considered the ‘‘aggressive’’ lipids leading to tumor necrosis factor alpha (TNFa)-mediated liver damage and reactive oxygen species (ROS) formation.(19,20) These lipids could also be present in a nonsteatotic liver a”