Free fatty acids promote hepatic lipotoxicity by stimulating TNF‐α expression via a lysosomal pathway

By A. Feldstein, N. Werneburg, Ali Canbay, M. E. Guicciardi, S. Bronk, R. Rydzewski, L. Burgart, G. Gores. 2004

740 citations recorded by the source corpus.

Subfields: Cell Biology, Epidemiology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/9c305f03243d40cc0e497c5bc60fe24778edb10c

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In Cell Biology

1. Guido Kroemer
2. P. Boya
3. G. Hotamışlıgil
4. Beth Levine
5. C. Hetz

In Epidemiology

1. Guido Kroemer
2. A. Sanyal
3. P. Boya
4. B. Neuschwander‐Tetri
5. C. Day
6. E. Brunt
7. S. Bellentani
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In Molecular Biology

1. P. Boya
2. Guido Kroemer
3. B. Neuschwander‐Tetri
4. R. Ross
5. G. FitzGerald
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7. G. Hotamışlıgil
8. L. Galluzzi

Citations in the corpus

• Hepatic lipotoxicity and the pathogenesis of nonalcoholic steatohepatitis: The central role of nontriglyceride fatty acid metabolites (2010, background): “Fatty acids are also capable of directly destabilizing lysosomal membranes, leading to inappropriate release of cathepsin B and causing activation of apoptotic pathways.(49,50) As ligands for peroxisome proliferator-activated receptor alpha (PPARa), PPARc, and G protein–coupled receptors, fatty acid”
• The interaction of hepatic lipid and glucose metabolism in liver diseases. (2012, background): “FAs have been found to activate Toll-like receptors and initiate the extrinsic apoptosis cascade [91,92].”
• Lysosomal membrane permeabilization in cell death (2008, background): “Free fatty acids and bile salts can also induce LMPdependent cell death (Roberts et al., 1997; Feldstein et al., 2004, 2006).”
• Nonalcoholic fatty liver disease: pathology and pathogenesis. (2010, background): “The latter is a TNF-α pathway (118), and the former is a mitochondrial or a lysosomal pathway involving either JNK-dependent activation of the proapoptotic protein Bax or direct Bax activation, respectively (133).”
• Health Implications of High Dietary Omega-6 Polyunsaturated Fatty Acids (2012, background): “The accumulation of NEFAs within hepatocytes of NAFLD patients is another source of NFκB activation [104].”
• A position statement on NAFLD/NASH based on the EASL 2009 special conference. (2010, background): “Oxidative stress [144] and gut flora/cytokines [145] can induce steatosis as well as necroinflammation and fibrosis.”
• INCREASED HEPATIC SYNTHESIS AND DYSREGULATION OF CHOLESTEROL METABOLISM IS ASSOCIATED WITH THE SEVERITY OF NONALCOHOLIC FATTY LIVER DISEASE (2012, background): “Prior studies have focused on the role of free fatty acids as a key driver of lipotoxicity in NAFLD and support the concept that triglyceride synthesis diminishes fatty acid toxicity by acting as a sump to limit fatty acid accumulation (Feldstein et al., 2004; Yamaguchi et al., 2008).”