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- W2805890278 abstract "Cholesterol is the only lipid whose absorption in the gastrointestinal tract is limited by gate-keeping transporters and efflux mechanisms, preventing its rapid absorption and accumulation in the liver and blood vessels. In this review, I explored the current data regarding cholesterol accumulation in liver cells and key mechanisms in cholesterol-induced fatty liver disease associated with the activation of deleterious hypoxic and nitric oxide signal transduction pathways. Although nonalcoholic fatty liver disease (NAFLD) affects both obese and nonobese individuals, the mechanism of NAFLD progression in lean individuals with healthy metabolism is puzzling. Lean NAFLD individuals exhibit normal metabolic responses, implying that liver damage is not associated with impaired metabolism per se and that direct lipotoxic effects are crucial for disease progression. Several redox and oxidant signaling pathways involving cholesterol are at play in fatty liver disease development. These include impairment of the mitochondrial and lysosomal function by cholesterol loading of the inner-cell membranes; formation of cholesterol crystals and hepatocyte degradation; and crown-like structures surrounding degrading hepatocytes, activating Kupffer cells, and evoking inflammation. The current review focuses on the induction of liver inflammation, fibrosis, and steatosis by free cholesterol via the hypoxia-inducible factor 1 α (HIF-1 α ), a main oxygen-sensing transcription factor involved in all stages of NAFLD. Cholesterol loading in hepatocytes can result in chronic HIF-1 α activity because of the decreased oxygen availability and excessive production of nitric oxide and mitochondrial reactive oxygen species." @default.
- W2805890278 created "2018-06-13" @default.
- W2805890278 creator A5031288153 @default.
- W2805890278 date "2018-05-31" @default.
- W2805890278 modified "2023-10-12" @default.
- W2805890278 title "Hypoxic Signaling and Cholesterol Lipotoxicity in Fatty Liver Disease Progression" @default.
- W2805890278 cites W1503760388 @default.
- W2805890278 cites W1551034491 @default.
- W2805890278 cites W1820959305 @default.
- W2805890278 cites W1852430852 @default.
- W2805890278 cites W1874465904 @default.
- W2805890278 cites W1911024010 @default.
- W2805890278 cites W1967972402 @default.
- W2805890278 cites W1977194186 @default.
- W2805890278 cites W1980825418 @default.
- W2805890278 cites W1984178243 @default.
- W2805890278 cites W1984661645 @default.
- W2805890278 cites W1985333297 @default.
- W2805890278 cites W1994261934 @default.
- W2805890278 cites W1995541025 @default.
- W2805890278 cites W1995743412 @default.
- W2805890278 cites W1996263427 @default.
- W2805890278 cites W1996266503 @default.
- W2805890278 cites W1998907758 @default.
- W2805890278 cites W2003749614 @default.
- W2805890278 cites W2003979065 @default.
- W2805890278 cites W2007492445 @default.
- W2805890278 cites W2008727369 @default.
- W2805890278 cites W2010101404 @default.
- W2805890278 cites W2015087574 @default.
- W2805890278 cites W2017025391 @default.
- W2805890278 cites W2019560452 @default.
- W2805890278 cites W2019712940 @default.
- W2805890278 cites W2019714748 @default.
- W2805890278 cites W2020425332 @default.
- W2805890278 cites W2024429100 @default.
- W2805890278 cites W2024639496 @default.
- W2805890278 cites W2024838891 @default.
- W2805890278 cites W2026244691 @default.
- W2805890278 cites W2028841855 @default.
- W2805890278 cites W2038681065 @default.
- W2805890278 cites W2039559614 @default.
- W2805890278 cites W2039630990 @default.
- W2805890278 cites W2042778710 @default.
- W2805890278 cites W2042981158 @default.
- W2805890278 cites W2043433914 @default.
- W2805890278 cites W2043446648 @default.
- W2805890278 cites W2044448807 @default.
- W2805890278 cites W2048599809 @default.
- W2805890278 cites W2055902411 @default.
- W2805890278 cites W2058753526 @default.
- W2805890278 cites W2063088635 @default.
- W2805890278 cites W2064431177 @default.
- W2805890278 cites W2066784926 @default.
- W2805890278 cites W2070053386 @default.
- W2805890278 cites W2072451938 @default.
- W2805890278 cites W2073438109 @default.
- W2805890278 cites W2083322721 @default.
- W2805890278 cites W2092412521 @default.
- W2805890278 cites W2098906667 @default.
- W2805890278 cites W2106069121 @default.
- W2805890278 cites W2108573150 @default.
- W2805890278 cites W2108848054 @default.
- W2805890278 cites W2109538419 @default.
- W2805890278 cites W2114233282 @default.
- W2805890278 cites W2115817322 @default.
- W2805890278 cites W2119863741 @default.
- W2805890278 cites W2130292454 @default.
- W2805890278 cites W2134247216 @default.
- W2805890278 cites W2135450217 @default.
- W2805890278 cites W2137508759 @default.
- W2805890278 cites W2139776835 @default.
- W2805890278 cites W2141847116 @default.
- W2805890278 cites W2144178804 @default.
- W2805890278 cites W2144297117 @default.
- W2805890278 cites W2146720979 @default.
- W2805890278 cites W2155259249 @default.
- W2805890278 cites W2163484250 @default.
- W2805890278 cites W2163823536 @default.
- W2805890278 cites W2164249299 @default.
- W2805890278 cites W2188065204 @default.
- W2805890278 cites W2205982384 @default.
- W2805890278 cites W2253667517 @default.
- W2805890278 cites W2256440089 @default.
- W2805890278 cites W2264982161 @default.
- W2805890278 cites W2273379630 @default.
- W2805890278 cites W2279591026 @default.
- W2805890278 cites W2304266037 @default.
- W2805890278 cites W2336816986 @default.
- W2805890278 cites W2411583672 @default.
- W2805890278 cites W2412473917 @default.
- W2805890278 cites W2416352929 @default.
- W2805890278 cites W2469365710 @default.
- W2805890278 cites W2498475603 @default.
- W2805890278 cites W2511630563 @default.
- W2805890278 cites W2521475965 @default.
- W2805890278 cites W2552872119 @default.
- W2805890278 cites W2555699543 @default.