An AMPK–caspase-6 axis controls liver damage in nonalcoholic steatohepatitis | Zendy

Peng Zhao | Zendy; Xiaoli Sun | Zendy; Cynthia Chaggan | Zendy; Zhongji Liao | Zendy; Kai in Wong | Zendy; Feng He | Zendy; Seema Singh | Zendy; Rohit Loomba | Zendy; Michael Karin | Zendy; Joseph L. Witztum | Zendy; Alan R. Saltiel | Zendy

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An AMPK–caspase-6 axis controls liver damage in nonalcoholic steatohepatitis

Author(s) -

Peng Zhao,

Xiaoli Sun,

Cynthia Chaggan,

Zhongji Liao,

Kai in Wong,

Feng He,

Seema Singh,

Rohit Loomba,

Michael Karin,

Joseph L. Witztum,

Alan R. Saltiel

Publication year - 2020

Publication title -

science

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 12.556

H-Index - 1186

eISSN - 1095-9203

pISSN - 0036-8075

DOI - 10.1126/science.aay0542

Subject(s) - ampk , nonalcoholic steatohepatitis , steatohepatitis , protein kinase a , amp activated protein kinase , adenosine monophosphate , nonalcoholic fatty liver disease , apoptosis , liver injury , fatty liver , chemistry , medicine , phosphorylation , cancer research , endocrinology , disease , biochemistry , adenosine

Liver disease defect identified The energy sensor adenosine monophosphate–activated protein kinase (AMPK) is implicated in liver damage in nonalcoholic steatohepatitis (NASH), a leading cause of liver-associated death in humans. Zhaoet al. used mouse models of NASH and samples from human NASH patients to show that AMPK, the activity of which is lost in NASH, phosphorylates the enzyme procaspase-6. In normal liver cells, this modification limits the activation of caspase-6 and the consequent caspase activation cascade that leads to apoptosis. AMPK and caspase-6 may thus provide therapeutic targets for the treatment of NASH.Science , this issue p.652

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