This review summarizes the multifactorial pathogenesis of NASH, highlighting the roles of insulin resistance, oxidative stress, and mitochondrial dysfunction.
Highlights multifactorial NASH pathogenesis for holistic evaluation; leaves open dominant pathway targeting in prospective trials.
Nonalcoholic fatty liver disease (NAFLD) represents a spectrum of liver diseases that range from hepatic steatosis at the most clinically benign end of the spectrum, through an intermediate lesion, nonalcoholic steatohepatitis (NASH), to cirrhosis at the opposite extreme. Epidemiology studies have estimated that about 20-30% of adults in the United States and other Western countries have NAFLD, and of these about 10% (2-3% of adults) meet the diagnostic criteria of NASH. Studies of animals and humans with obesity-related fatty liver disease have revealed much about the mechanisms that mediate this common pathology. The pathogenesis of NASH is multifactorial and includes insulin resistance, excessive intracellular fatty acids, oxidant stress, mitochondrial dysfunction and the role of innate immunity. This review will briefly discuss the epidemiology of NAFLD and focus on current understanding of the pathogenesis of NASH.
No takes yet. Share an insight, caveat, or question.
Ma et al. (2006) studied this question.
Synapse has enriched 4 closely related papers on similar clinical questions. Consider them for comparative context: