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• W3210185890 abstract "Chronic high-dose alcohol consumption impairs bone remodeling, reduces bone mass, and increases the risk of osteoporosis and bone fracture. However, the mechanisms underlying alcohol-induced osteoporosis are yet to be elucidated. In this study, we showed that excess intake of ethyl alcohol (EtOH) resulted in osteopenia and osteoblast necroptosis in mice that led to necrotic lesions and reduced osteogenic differentiation in bone marrow mesenchymal stem cells (BMMSCs). We found that EtOH treatment led to the activation of the RIPK1/RIPK3/MLKL signaling, resulting in increased osteoblast necroptosis and decreased osteogenic differentiation and bone formation both in vivo and in vitro. We further discovered that excessive EtOH treatment-induced osteoblast necroptosis might partly depend on reactive oxygen species (ROS) generation; concomitantly, ROS contributed to necroptosis of osteoblasts through a positive feedback loop involving RIPK1/RIPK3. In addition, blocking of the RIPK1/RIPK3/MLKL signaling by necrostatin-1 (Nec-1), a key inhibitor of RIPK1 kinase in the necroptosis pathway, or antioxidant N-acetylcysteine (NAC), an inhibitor of ROS, could decrease the activation of osteoblast necroptosis and ameliorate alcohol-induced osteopenia both in vivo and in vitro. Collectively, we demonstrated that chronic high-dose alcohol consumption induced osteopenia via osteoblast necroptosis and revealed that RIPK1 kinase may be a therapeutic target for alcohol-induced osteopenia." @default.
• W3210185890 created "2021-11-08" @default.
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• W3210185890 date "2021-10-27" @default.
• W3210185890 modified "2023-10-10" @default.
• W3210185890 title "Chronic Ethanol Consumption Induces Osteopenia via Activation of Osteoblast Necroptosis" @default.
• W3210185890 cites W1035050697 @default.
• W3210185890 cites W1523845694 @default.
• W3210185890 cites W1850224498 @default.
• W3210185890 cites W1966144041 @default.
• W3210185890 cites W1969323641 @default.
• W3210185890 cites W1972567404 @default.
• W3210185890 cites W1976866468 @default.
• W3210185890 cites W1976984647 @default.
• W3210185890 cites W1977446576 @default.
• W3210185890 cites W1979209029 @default.
• W3210185890 cites W1981477029 @default.
• W3210185890 cites W1982863111 @default.
• W3210185890 cites W1985792013 @default.
• W3210185890 cites W1988364018 @default.
• W3210185890 cites W1988592536 @default.
• W3210185890 cites W1990684374 @default.
• W3210185890 cites W1991997670 @default.
• W3210185890 cites W1993640536 @default.
• W3210185890 cites W1996180037 @default.
• W3210185890 cites W1998983498 @default.
• W3210185890 cites W2005928313 @default.
• W3210185890 cites W2010766264 @default.
• W3210185890 cites W2011828467 @default.
• W3210185890 cites W2016863921 @default.
• W3210185890 cites W2023122823 @default.
• W3210185890 cites W2032430933 @default.
• W3210185890 cites W2033968700 @default.
• W3210185890 cites W2035004863 @default.
• W3210185890 cites W2035806681 @default.
• W3210185890 cites W2060638067 @default.
• W3210185890 cites W2066659219 @default.
• W3210185890 cites W2067318843 @default.
• W3210185890 cites W2068659212 @default.
• W3210185890 cites W2077317536 @default.
• W3210185890 cites W2077479785 @default.
• W3210185890 cites W2086665516 @default.
• W3210185890 cites W2091263717 @default.
• W3210185890 cites W2094856707 @default.
• W3210185890 cites W2096425957 @default.
• W3210185890 cites W2104421483 @default.
• W3210185890 cites W2107411016 @default.
• W3210185890 cites W2145361436 @default.
• W3210185890 cites W2156807513 @default.
• W3210185890 cites W2158662692 @default.
• W3210185890 cites W2159256518 @default.
• W3210185890 cites W2159999899 @default.
• W3210185890 cites W2160651627 @default.
• W3210185890 cites W2164653101 @default.
• W3210185890 cites W2313673863 @default.
• W3210185890 cites W2345888432 @default.
• W3210185890 cites W2401425325 @default.
• W3210185890 cites W2418107622 @default.
• W3210185890 cites W2478800195 @default.
• W3210185890 cites W2480295405 @default.
• W3210185890 cites W2556795810 @default.
• W3210185890 cites W2558370604 @default.
• W3210185890 cites W2565402466 @default.
• W3210185890 cites W2586088194 @default.
• W3210185890 cites W2610328326 @default.
• W3210185890 cites W2789098190 @default.
• W3210185890 cites W2802280917 @default.
• W3210185890 cites W2890337997 @default.
• W3210185890 cites W2901813822 @default.
• W3210185890 cites W2904356101 @default.
• W3210185890 cites W2940129068 @default.
• W3210185890 cites W2942761172 @default.
• W3210185890 cites W2950937606 @default.
• W3210185890 cites W2954850953 @default.
• W3210185890 cites W2970671727 @default.
• W3210185890 cites W2972960041 @default.
• W3210185890 cites W2981958006 @default.
• W3210185890 cites W2991483425 @default.
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• W3210185890 doi "https://doi.org/10.1155/2021/3027954" @default.
• W3210185890 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/8566044" @default.
• W3210185890 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/34745415" @default.
• W3210185890 hasPublicationYear "2021" @default.
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