MicroRNAs: Unfolding the link between inositol‐requiring enzyme 1α and fatty liver

Abstract

Nonalcoholic fatty liver disease (NAFLD) is currently the most common cause of abnormal liver chemistry tests in the United States and western world. The mechanisms underlying hepatic steatosis and the progression to nonalcoholic steatohepatitis (NASH) remain incompletely understood. Multiple cellular stress pathways are believed to contribute to the pathogenesis of fatty liver, including endoplasmic reticulum (ER) stress and its adaptive unfolded protein response (UPR). Numerous studies have demonstrated the important role of ER stress and UPR activation in a host of liver diseases including viral hepatitis, alcohol and drug hepatotoxicity, cholestatic liver disorders and genetic liver diseases.

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