Abstract:
Fatty liver disease constitutes a spectrum of liver diseases which begin with simple steatosis and
may progress to advance stages of steatohepatitis, cirrhosis, and hepatocellular carcinoma (HCC). The two
main etiologies are—alcohol related fatty liver disease (ALD) and nonalcoholic fatty liver disease (NAFLD).
NAFLD is a global health epidemic strongly associated with modern dietary habits and life-style. It is
the second most common cause of chronic liver disease in the US after chronic hepatitis C virus (HCV)
infection. Approximately 100 million people are affected with this condition in the US alone. Excessive
intakes of calories, saturated fat and refined carbohydrates, and sedentary life style have led to explosion
of this health epidemic in developing nations as well. ALD is the third most common cause of chronic
liver disease in the US. Even though the predominant trigger for onset of steatosis is different in these two
conditions, they share common themes in progression from steatosis to the advance stages. Oxidative stress
(OS) is considered a very significant contributor to hepatocyte injury in these conditions. Mitochondrial
dysfunction contributes to this OS. Role of mitochondrial dysfunction in pathogenesis of fatty liver diseases
is emerging but far from completely understood. A better understanding is essential for more effective
preventive and therapeutic interventions. Here, we discuss the pathogenesis and therapeutic approaches of
NAFLD and ALD from a mitochondrial perspective.
Keywords: Mitochondria; nonalcoholic fatty liver disease (NAFLD); nonalcoholic steatohepatitis (NASH);
metabolic syndrome; mitochondrial dysfunction
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