Nonalcoholic fatty liver disease: pathology and pathogenesis.

By D. Tiniakos, M. Vos, E. Brunt. Annual Review of Pathology, 2010

841 citations recorded by the source corpus.

How researchers see this paper

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

Fatty Acid and Endotoxin Activate Inflammasomes in Mouse Hepatocytes that Release Danger Signals to Stimulate Immune Cells (2011, neutral): “N onalcoholic fatty liver disease (NAFLD) is one of the most common liver diseases and affects more than one-third of the population of the Western world.(1,2) The histopathological spectrum of NAFLD includes steatosis alone, steatosis with inflammation, and steatohepatitis with necroinflammation (w”
Bile Acid Signaling in Metabolic Disease and Drug Therapy (2014, neutral): “(Farrell and Larter, 2006; Tiniakos et al., 2010).”
Evolution of inflammation in nonalcoholic fatty liver disease: The multiple parallel hits hypothesis (2010, background): “Insulin resistance may augment inflammation in NASH because patients with type 2 diabetes mellitus are often worse in terms of histopathological changes such as ballooning, apoptosis, and lobular and/or portal inflammation.(1) Serine phosphorylation of insulin receptor substrate by inflammatory sign”
Oxidative Stress in Obesity: A Critical Component in Human Diseases (2014, background): “model” is the most widespread: The first hit is insulin resistant promoting hepatic fat accumulation, and the second hit, through a large number of adipokines (leptin, adiponectin, resistin), is sustained by FFAs that induce ROS injury [114].”