Hepatocyte apoptosis and fas expression are prominent features of human nonalcoholic steatohepatitis.

By A. Feldstein, Ali Canbay, P. Angulo, M. Taniai, L. Burgart, K. Lindor, G. Gores. Gastroenterology, 2003

1,046 citations recorded by the source corpus.

Subfields: Epidemiology, Hepatology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/926ecc5b21f5579fa80f61ecd2b4d334c8060960

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Epidemiology

1. C. Hetz
2. É. Chevet
3. Ali Canbay
4. M. Trauner
5. G. Gerken
6. Rebekka A. Hannivoort
7. L. Bechmann
8. R. Lopez

In Hepatology

1. R. Lopez
2. Natascha Roehlen
3. E. Crouchet
4. T. Baumert

In Pathology and Forensic Medicine

1. R. Lopez

Citations in the corpus

• Increased Hepatic and Circulating Interleukin-6 Levels in Human Nonalcoholic Steatohepatitis (2008, methodology): “Age (yr) 49 (12) 54 (8) 46 (16) 40 (9) 0.”
• Mitochondrial Glutathione, a Key Survival Antioxidant (2009, background): “ASH and nonalcoholic steatohepatitis (NASH) are two of the most common forms of liver disease worldwide and represent an advanced stage in the spectrum of fatty liver diseases.”
• Mitochondrial DNA in inflammation and immunity (2020, neutral): “NASH is characterised by different forms of cell death, most prominently apoptosis [184] and necrosis [185,186].”
• The interaction of hepatic lipid and glucose metabolism in liver diseases. (2012, background): “FAs themselves also promote hepatic IR via TNF receptor activation, hence indicating a vicious circle of lipid accumulation and IR as a crucial mechanism in the pathogenesis of NASH (Fig.”
• From pyroptosis, apoptosis and necroptosis to PANoptosis: A mechanistic compendium of programmed cell death pathways (2021, background): “Similar involvement of key PANopto-some molecules and pyroptosis, apoptosis and necroptosis are also seen in metabolic diseases [160–163].”
• Saturated fatty acids induce endoplasmic reticulum stress and apoptosis independently of ceramide in liver cells. (2006, background): “Notably, activation of JNK can lead to apoptosis (5, 19), and hepatocyte apoptosis appears to be increased in patients with NASH and correlates with disease severity (9).”
• Liver Fibrosis: Mechanistic Concepts and Therapeutic Perspectives (2020, background): “However, a pro-fibrogenic response can be elicited by hepatocyte apoptosis through activation of the Fas death receptor [33,34].”