Role of oxidative stress in the pathogenesis of nonalcoholic steatohepatitis.

By A. Rolo, J. Teodoro, C. Palmeira. Free Radical Biology & Medicine, 2012

898 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.

Decoding cell death signals in liver inflammation. (2013, background): “Along similar lines, chemical inhibitors of ALOX5 or 5-lipoxygenase-activating protein (FLAP, an ALOX5 interactor) have been shown to reduce CCl4-induced liver injury [94] and to limit the inflammatory infiltration of the hepatic parenchyma in several distinct models of NASH and NAFLD [92], perhaps ”
Oxidative Stress in Obesity: A Critical Component in Human Diseases (2014, background): “The consequent increased generation of ROS and reactive aldehydic derivatives also promotes OS and cell death, via ATP, NAD, and glutathione depletion, and DNA, lipid, and protein damage [117].”
Obesity, Oxidative Stress, Adipose Tissue Dysfunction, and the Associated Health Risks: Causes and Therapeutic Strategies (2015, background): “The consequent overproduction of ROS and reactive aldehyde derivatives causes oxidative stress and cell death by reducing cellular ATP, NAD, and glutathione levels and causing DNA, lipid, and protein damage.(183) ER stress-induced cell death is mediated through calcium perturbations, ROS production,”
PGC-1α, Inflammation, and Oxidative Stress: An Integrative View in Metabolism (2020, background): “There is evidence to suggest that mitochondrial dysfunction and decreased fatty acid oxidation play a central role in the pathogenesis of NAFLD [202].”