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论文题目: MAPK1/3 regulate hepatic lipid metabolism via ATG7-dependent autophagy
英文论文题目: MAPK1/3 regulate hepatic lipid metabolism via ATG7-dependent autophagy
第一作者: Xiao, YZ; Liu, H; Yu, JJ; Zhao, ZL; Xiao, F; Xia, TT; Wang, CX; Li, K; Deng, JL; Guo, YJ; Chen, SH; Chen, Y; Guo, FF
英文第一作者: Xiao, YZ; Liu, H; Yu, JJ; Zhao, ZL; Xiao, F; Xia, TT; Wang, CX; Li, K; Deng, JL; Guo, YJ; Chen, SH; Chen, Y; Guo, FF
联系作者: Guo, FF (reprint author), 320 Yueyang Rd, Shanghai 200031, Peoples R China.
英文联系作者: Guo, FF (reprint author), 320 Yueyang Rd, Shanghai 200031, Peoples R China.
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发表年度: 2016
卷: 12
期: 3
页码: 592-593
摘要: Although many biological functions of MAPK1/ERK2-MAPK3/ERK1 (mitogen-activated protein kinase 1/3) have been reported, a direct effect of MAPK1/3 on hepatic lipid metabolism remains largely unknown. We recently showed that activation of MAPK1/3 ameliorates liver steatosis in LEPR (leptin receptor)-deficient (db/db) mice, a classic animal model for liver steatosis. Consistent with these results, knockdown of MAPK1/3 promotes liver steatosis in C57/B6J wild-type (WT) mice. Autophagic flux and ATG7 (autophagy related 7) levels are increased by MAPK1/3 activation or decreased by MAPK1/3 knockdown in livers and primary hepatocytes. Blockade of autophagic flux by chloroquine (CQ) or ATG7 knockdown reverses the ameliorated liver steatosis in MAPK1/3-activated db/db mice. Together, these findings identify a beneficial role for MAPK1/3 in liver steatosis that is mediated by ATG7-dependent autophagy, which provides novel insights into the mechanisms underlying liver steatosis and create a rationale for targeting MAPK1/3 in the treatment of liver steatosis.
英文摘要: Although many biological functions of MAPK1/ERK2-MAPK3/ERK1 (mitogen-activated protein kinase 1/3) have been reported, a direct effect of MAPK1/3 on hepatic lipid metabolism remains largely unknown. We recently showed that activation of MAPK1/3 ameliorates liver steatosis in LEPR (leptin receptor)-deficient (db/db) mice, a classic animal model for liver steatosis. Consistent with these results, knockdown of MAPK1/3 promotes liver steatosis in C57/B6J wild-type (WT) mice. Autophagic flux and ATG7 (autophagy related 7) levels are increased by MAPK1/3 activation or decreased by MAPK1/3 knockdown in livers and primary hepatocytes. Blockade of autophagic flux by chloroquine (CQ) or ATG7 knockdown reverses the ameliorated liver steatosis in MAPK1/3-activated db/db mice. Together, these findings identify a beneficial role for MAPK1/3 in liver steatosis that is mediated by ATG7-dependent autophagy, which provides novel insights into the mechanisms underlying liver steatosis and create a rationale for targeting MAPK1/3 in the treatment of liver steatosis.
刊物名称: AUTOPHAGY
英文刊物名称: AUTOPHAGY
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学科: Cell Biology
英文学科: Cell Biology
影响因子: 8.593
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论文类别: Article
英文论文类别: Article
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