Abstract
Toxic AGEs (TAGE) Theory in the Pathogenesis of NAFLD and ALD
Highlights
Nonalcoholic fatty liver disease (NAFLD) and alcoholic liver disease (ALD) are among the most common causes of chronic liver disease in the westernized world, which represents a worldwide public health problem [1]
There is a growing body of evidence to suggest that the interaction between GA-Advanced glycation end-products (AGEs), but not CML/CEL, and the receptor for AGEs (RAGE) may alter intracellular signaling, gene expression, and the release of pro-inflammatory molecules and elicits the generation of reactive oxygen species (ROS) in numerous types of cells, all of which may contribute to the pathological changes observed in diabetes mellitus (DM) and diabetic vascular complications, hypertension, cardiovascular disease (CVD), Alzheimer’s disease (AD), and cancer [18,19,20,21]
Steatosis simultaneously and completely disappeared after 12 weeks with the restoration of the lobular architecture of hepatic tissue [28]. These findings suggested that the Acetaldehyde-Derived AGEs (AA-AGEs) formed during the chronic consumption of ethanol could be eliminated after abstinence, which helped impaired hepatic tissue to return to its normal function
Summary
Nonalcoholic fatty liver disease (NAFLD) and alcoholic liver disease (ALD) are among the most common causes of chronic liver disease in the westernized world, which represents a worldwide public health problem [1]. The interaction between TAGE and the receptor for AGEs (RAGE) has been shown to alter intracellular signaling, gene expression and the release of pro-inflammatory molecules and elicits reactive oxygen species (ROS) in numerous types of cells, all of which may contribute to the pathological changes observed in lifestyle-related diseases.
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