Role and mechanisms of autophagy in acetaminophen-induced liver injury.
Role and mechanisms of autophagy in acetaminophen-induced liver injury.
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DOI:
10.1111/liv.13866
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发表时间:
2018-08
期刊:
影响因子:
--
通讯作者:
Ding WX
中科院分区:
文献类型:
--
作者:
Chao X;Wang H;Jaeschke H;Ding WX
Acetaminophen (APAP) overdose is the most frequent cause of acute liver failure in the United States and many other countries. Although the metabolism and pathogenesis of APAP has been extensively investigated for decades, the mechanisms by which APAP induces liver injury are incompletely known, which hampers the development of effective therapeutic approaches to tackle this important clinical problem. Autophagy is a highly conserved intracellular degradation pathway, which aims at recycling cellular components and damaged organelles in response to adverse environmental conditions and stresses as a survival mechanism. There is accumulating evidence indicating that autophagy is activated in response to APAP overdose in specific liver zone areas, and pharmacological activation of autophagy protects against APAP-induced liver injury. Increasing evidence also suggests that hepatic autophagy is impaired in nonalcoholic fatty livers (NAFLD), and NAFLD patients are more susceptible to APAP-induced liver injury. Here we summarized the current progress on the role and mechanisms of autophagy in protecting against APAP-induced liver injury.
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影响因子:
3.8
作者:
Du, Kuo;Williams, C. David;McGill, Mitchell R.;Jaeschke, Hartmut
通讯作者:
Jaeschke, Hartmut
DOI:
10.1186/1472-6904-12-11
发表时间:
2012-06-18
期刊:
BMC clinical pharmacology
影响因子:
--
作者:
Clark R;Fisher JE;Sketris IS;Johnston GM
通讯作者:
Johnston GM
影响因子:
29.7
作者:
Davis BK;Wen H;Ting JP
通讯作者:
Ting JP
DOI:
10.1126/science.1196371
发表时间:
2011-01-28
期刊:
Science (New York, N.Y.)
影响因子:
--
作者:
Egan DF;Shackelford DB;Mihaylova MM;Gelino S;Kohnz RA;Mair W;Vasquez DS;Joshi A;Gwinn DM;Taylor R;Asara JM;Fitzpatrick J;Dillin A;Viollet B;Kundu M;Hansen M;Shaw RJ
通讯作者:
Shaw RJ
影响因子:
4.8
作者:
Ding, Wen-Xing;Li, Min;Yin, Xiao-Ming
通讯作者:
Yin, Xiao-Ming