Advances in the Mechanism of Plateau Hypoxia Modulating the Induction of Non-alcoholic Fatty Liver Disease
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Published on: March 11, 2017
Minghui Zhao1,2, Hongfang Mu1, Ziqin Wei1,2
1Department of Pharmacy, The 940th Hospital of Joint Logistics Support Force of People's Liberation Army, Lanzhou 730050, China.
Abstract:
Non-alcoholic fatty liver disease (NAFLD) is a prevalent chronic liver condition that poses a significant threat to human health globally. Recent studies have established a strong correlation between liver diseases and hypoxic environments, revealing varying degrees of tissue hypoxia during the progression of NAFLD, chronic hepatitis, and cirrhosis. Liver tissue is susceptible to damage in low-oxygen environments, such as those found at high altitudes, which significantly increases the prevalence of NAFLD. Concurrently, hypoxia can induce oxidative stress, leading to insulin resistance (IR), mitochondrial dysfunction, inflammatory responses, and disturbances in intestinal flora. Changes in these levels can disrupt liver function, trigger lipid deposition, and ultimately lead to hepatocyte death. Additionally, the enhanced inflammatory response of various immune cells can further accelerate the progression of hepatic fibrosis, deepening the degree of hypoxia. This creates a vicious cycle that ultimately aggravates disease progression. By modifying dietary habits, avoiding hypoxic environments, providing appropriate treatment for drugs that affect IR, and rationally using medications that balance intestinal flora, effective strategies for preventing and improving NAFLD may be developed. In summary, this paper discusses the research progress related to plateau hypoxia and NAFLD, and it summarizes the prevention, diagnosis, and treatment of NAFLD in conjunction with its pathogenesis.
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