The Upstream Pathway of mTOR-Mediated Autophagy in Liver Diseases
Identifieur interne : 000930 ( Pmc/Curation ); précédent : 000929; suivant : 000931The Upstream Pathway of mTOR-Mediated Autophagy in Liver Diseases
Auteurs : Haojie Wang ; Yumei Liu ; Dongmei Wang ; Yaolu Xu ; Ruiqi Dong ; Yuxiang Yang ; Qiongxia Lv ; Xiaoguang Chen ; Ziqiang ZhangSource :
- Cells [ 2073-4409 ] ; 2019.
Abstract
Autophagy, originally found in liver experiments, is a cellular process that degrades damaged organelle or protein aggregation. This process frees cells from various stress states is a cell survival mechanism under stress stimulation. It is now known that dysregulation of autophagy can cause many liver diseases. Therefore, how to properly regulate autophagy is the key to the treatment of liver injury. mechanistic target of rapamycin (mTOR)is the core hub regulating autophagy, which is subject to different upstream signaling pathways to regulate autophagy. This review summarizes three upstream pathways of mTOR: the phosphoinositide 3-kinase (PI3K)/protein kinase (AKT) signaling pathway, the adenosine monophosphate-activated protein kinase (AMPK) signaling pathway, and the rat sarcoma (Ras)/rapidly accelerated fibrosarcoma (Raf)/mitogen-extracellular activated protein kinase kinase (MEK)/ extracellular-signal-regulated kinase (ERK) signaling pathway, specifically explored their role in liver fibrosis, hepatitis B, non-alcoholic fatty liver, liver cancer, hepatic ischemia reperfusion and other liver diseases through the regulation of mTOR-mediated autophagy. Moreover, we also analyzed the crosstalk between these three pathways, aiming to find new targets for the treatment of human liver disease based on autophagy.
Url:
DOI: 10.3390/cells8121597
PubMed: 31835352
PubMed Central: 6953127
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">The Upstream Pathway of mTOR-Mediated Autophagy in Liver Diseases</title><author><name sortKey="Wang, Haojie" sort="Wang, Haojie" uniqKey="Wang H" first="Haojie" last="Wang">Haojie Wang</name><affiliation><nlm:aff id="af1-cells-08-01597">College of Animal Science and Technology, Henan University of Science and Technology, Luoyang 471000, China;<email>haojiewang@stu.haust.edu.cn</email> (H.W.);<email>180218250878@stu.haust.edu.cn</email> (Y.X.);<email>180218250881@stu.haust.edu.cn</email> (R.D.);<email>yyxiang2018@126.com</email> (Y.Y.);<email>lvqx20001@163.com</email> (Q.L.);<email>cxguang1015@126.com</email> (X.C.)</nlm:aff></affiliation></author><author><name sortKey="Liu, Yumei" sort="Liu, Yumei" uniqKey="Liu Y" first="Yumei" last="Liu">Yumei Liu</name><affiliation><nlm:aff id="af1-cells-08-01597">College of Animal Science and Technology, Henan University of Science and Technology, Luoyang 471000, China;<email>haojiewang@stu.haust.edu.cn</email> (H.W.);<email>180218250878@stu.haust.edu.cn</email> (Y.X.);<email>180218250881@stu.haust.edu.cn</email> (R.D.);<email>yyxiang2018@126.com</email> (Y.Y.);<email>lvqx20001@163.com</email> (Q.L.);<email>cxguang1015@126.com</email> (X.C.)</nlm:aff></affiliation></author><author><name sortKey="Wang, Dongmei" sort="Wang, Dongmei" uniqKey="Wang D" first="Dongmei" last="Wang">Dongmei Wang</name><affiliation><nlm:aff id="af2-cells-08-01597">College of Medical, Henan University of Science and Technology, Luoyang 471000, China;<email>zzq828929@163.com</email></nlm:aff></affiliation></author><author><name sortKey="Xu, Yaolu" sort="Xu, Yaolu" uniqKey="Xu Y" first="Yaolu" last="Xu">Yaolu Xu</name><affiliation><nlm:aff id="af1-cells-08-01597">College of Animal Science and Technology, Henan University of Science and Technology, Luoyang 471000, China;<email>haojiewang@stu.haust.edu.cn</email> (H.W.);<email>180218250878@stu.haust.edu.cn</email> (Y.X.);<email>180218250881@stu.haust.edu.cn</email> (R.D.);<email>yyxiang2018@126.com</email> (Y.Y.);<email>lvqx20001@163.com</email> (Q.L.);<email>cxguang1015@126.com</email> (X.C.)</nlm:aff></affiliation></author><author><name sortKey="Dong, Ruiqi" sort="Dong, Ruiqi" uniqKey="Dong R" first="Ruiqi" last="Dong">Ruiqi Dong</name><affiliation><nlm:aff id="af1-cells-08-01597">College of Animal Science and Technology, Henan University of Science and Technology, Luoyang 471000, China;<email>haojiewang@stu.haust.edu.cn</email> (H.W.);<email>180218250878@stu.haust.edu.cn</email> (Y.X.);<email>180218250881@stu.haust.edu.cn</email> (R.D.);<email>yyxiang2018@126.com</email> (Y.Y.);<email>lvqx20001@163.com</email> (Q.L.);<email>cxguang1015@126.com</email> (X.C.)</nlm:aff></affiliation></author><author><name sortKey="Yang, Yuxiang" sort="Yang, Yuxiang" uniqKey="Yang Y" first="Yuxiang" last="Yang">Yuxiang Yang</name><affiliation><nlm:aff id="af1-cells-08-01597">College of Animal Science and Technology, Henan University of Science and Technology, Luoyang 471000, China;<email>haojiewang@stu.haust.edu.cn</email> (H.W.);<email>180218250878@stu.haust.edu.cn</email> (Y.X.);<email>180218250881@stu.haust.edu.cn</email> (R.D.);<email>yyxiang2018@126.com</email> (Y.Y.);<email>lvqx20001@163.com</email> (Q.L.);<email>cxguang1015@126.com</email> (X.C.)</nlm:aff></affiliation></author><author><name sortKey="Lv, Qiongxia" sort="Lv, Qiongxia" uniqKey="Lv Q" first="Qiongxia" last="Lv">Qiongxia Lv</name><affiliation><nlm:aff id="af1-cells-08-01597">College of Animal Science and Technology, Henan University of Science and Technology, Luoyang 471000, China;<email>haojiewang@stu.haust.edu.cn</email> (H.W.);<email>180218250878@stu.haust.edu.cn</email> (Y.X.);<email>180218250881@stu.haust.edu.cn</email> (R.D.);<email>yyxiang2018@126.com</email> (Y.Y.);<email>lvqx20001@163.com</email> (Q.L.);<email>cxguang1015@126.com</email> (X.C.)</nlm:aff></affiliation></author><author><name sortKey="Chen, Xiaoguang" sort="Chen, Xiaoguang" uniqKey="Chen X" first="Xiaoguang" last="Chen">Xiaoguang Chen</name><affiliation><nlm:aff id="af1-cells-08-01597">College of Animal Science and Technology, Henan University of Science and Technology, Luoyang 471000, China;<email>haojiewang@stu.haust.edu.cn</email> (H.W.);<email>180218250878@stu.haust.edu.cn</email> (Y.X.);<email>180218250881@stu.haust.edu.cn</email> (R.D.);<email>yyxiang2018@126.com</email> (Y.Y.);<email>lvqx20001@163.com</email> (Q.L.);<email>cxguang1015@126.com</email> (X.C.)</nlm:aff></affiliation></author><author><name sortKey="Zhang, Ziqiang" sort="Zhang, Ziqiang" uniqKey="Zhang Z" first="Ziqiang" last="Zhang">Ziqiang Zhang</name><affiliation><nlm:aff id="af1-cells-08-01597">College of Animal Science and Technology, Henan University of Science and Technology, Luoyang 471000, China;<email>haojiewang@stu.haust.edu.cn</email> (H.W.);<email>180218250878@stu.haust.edu.cn</email> (Y.X.);<email>180218250881@stu.haust.edu.cn</email> (R.D.);<email>yyxiang2018@126.com</email> (Y.Y.);<email>lvqx20001@163.com</email> (Q.L.);<email>cxguang1015@126.com</email> (X.C.)</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">31835352</idno><idno type="pmc">6953127</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6953127</idno><idno type="RBID">PMC:6953127</idno><idno type="doi">10.3390/cells8121597</idno><date when="2019">2019</date><idno type="wicri:Area/Pmc/Corpus">000930</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000930</idno><idno type="wicri:Area/Pmc/Curation">000930</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">000930</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">The Upstream Pathway of mTOR-Mediated Autophagy in Liver Diseases</title><author><name sortKey="Wang, Haojie" sort="Wang, Haojie" uniqKey="Wang H" first="Haojie" last="Wang">Haojie Wang</name><affiliation><nlm:aff id="af1-cells-08-01597">College of Animal Science and Technology, Henan University of Science and Technology, Luoyang 471000, China;<email>haojiewang@stu.haust.edu.cn</email> (H.W.);<email>180218250878@stu.haust.edu.cn</email> (Y.X.);<email>180218250881@stu.haust.edu.cn</email> (R.D.);<email>yyxiang2018@126.com</email> (Y.Y.);<email>lvqx20001@163.com</email> (Q.L.);<email>cxguang1015@126.com</email> (X.C.)</nlm:aff></affiliation></author><author><name sortKey="Liu, Yumei" sort="Liu, Yumei" uniqKey="Liu Y" first="Yumei" last="Liu">Yumei Liu</name><affiliation><nlm:aff id="af1-cells-08-01597">College of Animal Science and Technology, Henan University of Science and Technology, Luoyang 471000, China;<email>haojiewang@stu.haust.edu.cn</email> (H.W.);<email>180218250878@stu.haust.edu.cn</email> (Y.X.);<email>180218250881@stu.haust.edu.cn</email> (R.D.);<email>yyxiang2018@126.com</email> (Y.Y.);<email>lvqx20001@163.com</email> (Q.L.);<email>cxguang1015@126.com</email> (X.C.)</nlm:aff></affiliation></author><author><name sortKey="Wang, Dongmei" sort="Wang, Dongmei" uniqKey="Wang D" first="Dongmei" last="Wang">Dongmei Wang</name><affiliation><nlm:aff id="af2-cells-08-01597">College of Medical, Henan University of Science and Technology, Luoyang 471000, China;<email>zzq828929@163.com</email></nlm:aff></affiliation></author><author><name sortKey="Xu, Yaolu" sort="Xu, Yaolu" uniqKey="Xu Y" first="Yaolu" last="Xu">Yaolu Xu</name><affiliation><nlm:aff id="af1-cells-08-01597">College of Animal Science and Technology, Henan University of Science and Technology, Luoyang 471000, China;<email>haojiewang@stu.haust.edu.cn</email> (H.W.);<email>180218250878@stu.haust.edu.cn</email> (Y.X.);<email>180218250881@stu.haust.edu.cn</email> (R.D.);<email>yyxiang2018@126.com</email> (Y.Y.);<email>lvqx20001@163.com</email> (Q.L.);<email>cxguang1015@126.com</email> (X.C.)</nlm:aff></affiliation></author><author><name sortKey="Dong, Ruiqi" sort="Dong, Ruiqi" uniqKey="Dong R" first="Ruiqi" last="Dong">Ruiqi Dong</name><affiliation><nlm:aff id="af1-cells-08-01597">College of Animal Science and Technology, Henan University of Science and Technology, Luoyang 471000, China;<email>haojiewang@stu.haust.edu.cn</email> (H.W.);<email>180218250878@stu.haust.edu.cn</email> (Y.X.);<email>180218250881@stu.haust.edu.cn</email> (R.D.);<email>yyxiang2018@126.com</email> (Y.Y.);<email>lvqx20001@163.com</email> (Q.L.);<email>cxguang1015@126.com</email> (X.C.)</nlm:aff></affiliation></author><author><name sortKey="Yang, Yuxiang" sort="Yang, Yuxiang" uniqKey="Yang Y" first="Yuxiang" last="Yang">Yuxiang Yang</name><affiliation><nlm:aff id="af1-cells-08-01597">College of Animal Science and Technology, Henan University of Science and Technology, Luoyang 471000, China;<email>haojiewang@stu.haust.edu.cn</email> (H.W.);<email>180218250878@stu.haust.edu.cn</email> (Y.X.);<email>180218250881@stu.haust.edu.cn</email> (R.D.);<email>yyxiang2018@126.com</email> (Y.Y.);<email>lvqx20001@163.com</email> (Q.L.);<email>cxguang1015@126.com</email> (X.C.)</nlm:aff></affiliation></author><author><name sortKey="Lv, Qiongxia" sort="Lv, Qiongxia" uniqKey="Lv Q" first="Qiongxia" last="Lv">Qiongxia Lv</name><affiliation><nlm:aff id="af1-cells-08-01597">College of Animal Science and Technology, Henan University of Science and Technology, Luoyang 471000, China;<email>haojiewang@stu.haust.edu.cn</email> (H.W.);<email>180218250878@stu.haust.edu.cn</email> (Y.X.);<email>180218250881@stu.haust.edu.cn</email> (R.D.);<email>yyxiang2018@126.com</email> (Y.Y.);<email>lvqx20001@163.com</email> (Q.L.);<email>cxguang1015@126.com</email> (X.C.)</nlm:aff></affiliation></author><author><name sortKey="Chen, Xiaoguang" sort="Chen, Xiaoguang" uniqKey="Chen X" first="Xiaoguang" last="Chen">Xiaoguang Chen</name><affiliation><nlm:aff id="af1-cells-08-01597">College of Animal Science and Technology, Henan University of Science and Technology, Luoyang 471000, China;<email>haojiewang@stu.haust.edu.cn</email> (H.W.);<email>180218250878@stu.haust.edu.cn</email> (Y.X.);<email>180218250881@stu.haust.edu.cn</email> (R.D.);<email>yyxiang2018@126.com</email> (Y.Y.);<email>lvqx20001@163.com</email> (Q.L.);<email>cxguang1015@126.com</email> (X.C.)</nlm:aff></affiliation></author><author><name sortKey="Zhang, Ziqiang" sort="Zhang, Ziqiang" uniqKey="Zhang Z" first="Ziqiang" last="Zhang">Ziqiang Zhang</name><affiliation><nlm:aff id="af1-cells-08-01597">College of Animal Science and Technology, Henan University of Science and Technology, Luoyang 471000, China;<email>haojiewang@stu.haust.edu.cn</email> (H.W.);<email>180218250878@stu.haust.edu.cn</email> (Y.X.);<email>180218250881@stu.haust.edu.cn</email> (R.D.);<email>yyxiang2018@126.com</email> (Y.Y.);<email>lvqx20001@163.com</email> (Q.L.);<email>cxguang1015@126.com</email> (X.C.)</nlm:aff></affiliation></author></analytic><series><title level="j">Cells</title><idno type="eISSN">2073-4409</idno><imprint><date when="2019">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Autophagy, originally found in liver experiments, is a cellular process that degrades damaged organelle or protein aggregation. This process frees cells from various stress states is a cell survival mechanism under stress stimulation. It is now known that dysregulation of autophagy can cause many liver diseases. Therefore, how to properly regulate autophagy is the key to the treatment of liver injury. mechanistic target of rapamycin (mTOR)is the core hub regulating autophagy, which is subject to different upstream signaling pathways to regulate autophagy. This review summarizes three upstream pathways of mTOR: the phosphoinositide 3-kinase (PI3K)/protein kinase (AKT) signaling pathway, the adenosine monophosphate-activated protein kinase (AMPK) signaling pathway, and the rat sarcoma (Ras)/rapidly accelerated fibrosarcoma (Raf)/mitogen-extracellular activated protein kinase kinase (MEK)/ extracellular-signal-regulated kinase (ERK) signaling pathway, specifically explored their role in liver fibrosis, hepatitis B, non-alcoholic fatty liver, liver cancer, hepatic ischemia reperfusion and other liver diseases through the regulation of mTOR-mediated autophagy. Moreover, we also analyzed the crosstalk between these three pathways, aiming to find new targets for the treatment of human liver disease based on autophagy.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Trefts, E" uniqKey="Trefts E">E. Trefts</name></author><author><name sortKey="Gannon, M" uniqKey="Gannon M">M. 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Cells</journal-id><journal-id journal-id-type="iso-abbrev">Cells</journal-id><journal-id journal-id-type="publisher-id">cells</journal-id><journal-title-group><journal-title>Cells</journal-title></journal-title-group><issn pub-type="epub">2073-4409</issn><publisher><publisher-name>MDPI</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">31835352</article-id><article-id pub-id-type="pmc">6953127</article-id><article-id pub-id-type="doi">10.3390/cells8121597</article-id><article-id pub-id-type="publisher-id">cells-08-01597</article-id><article-categories><subj-group subj-group-type="heading"><subject>Review</subject></subj-group></article-categories><title-group><article-title>The Upstream Pathway of mTOR-Mediated Autophagy in Liver Diseases</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Wang</surname><given-names>Haojie</given-names></name><xref ref-type="aff" rid="af1-cells-08-01597">1</xref></contrib><contrib contrib-type="author"><name><surname>Liu</surname><given-names>Yumei</given-names></name><xref ref-type="aff" rid="af1-cells-08-01597">1</xref><xref rid="c1-cells-08-01597" ref-type="corresp">*</xref></contrib><contrib contrib-type="author"><name><surname>Wang</surname><given-names>Dongmei</given-names></name><xref ref-type="aff" rid="af2-cells-08-01597">2</xref></contrib><contrib contrib-type="author"><name><surname>Xu</surname><given-names>Yaolu</given-names></name><xref ref-type="aff" rid="af1-cells-08-01597">1</xref></contrib><contrib contrib-type="author"><name><surname>Dong</surname><given-names>Ruiqi</given-names></name><xref ref-type="aff" rid="af1-cells-08-01597">1</xref></contrib><contrib contrib-type="author"><name><surname>Yang</surname><given-names>Yuxiang</given-names></name><xref ref-type="aff" rid="af1-cells-08-01597">1</xref></contrib><contrib contrib-type="author"><name><surname>Lv</surname><given-names>Qiongxia</given-names></name><xref ref-type="aff" rid="af1-cells-08-01597">1</xref></contrib><contrib contrib-type="author"><name><surname>Chen</surname><given-names>Xiaoguang</given-names></name><xref ref-type="aff" rid="af1-cells-08-01597">1</xref></contrib><contrib contrib-type="author"><name><surname>Zhang</surname><given-names>Ziqiang</given-names></name><xref ref-type="aff" rid="af1-cells-08-01597">1</xref><xref rid="c1-cells-08-01597" ref-type="corresp">*</xref></contrib></contrib-group><aff id="af1-cells-08-01597"><label>1</label>College of Animal Science and Technology, Henan University of Science and Technology, Luoyang 471000, China;<email>haojiewang@stu.haust.edu.cn</email> (H.W.);<email>180218250878@stu.haust.edu.cn</email> (Y.X.);<email>180218250881@stu.haust.edu.cn</email> (R.D.);<email>yyxiang2018@126.com</email> (Y.Y.);<email>lvqx20001@163.com</email> (Q.L.);<email>cxguang1015@126.com</email> (X.C.)</aff><aff id="af2-cells-08-01597"><label>2</label>College of Medical, Henan University of Science and Technology, Luoyang 471000, China;<email>zzq828929@163.com</email></aff><author-notes><corresp id="c1-cells-08-01597"><label>*</label>Correspondence: <email>yumeiliu@haust.edu.cn</email> (Y.L.); <email>ziqiangzhang@haust.edu.cn</email> (Z.Z.); Tel.: +86-153-2461-7957 (Y.L.); +86-153-0379-1931 (Z.Z.)</corresp></author-notes><pub-date pub-type="epub"><day>09</day><month>12</month><year>2019</year></pub-date><pub-date pub-type="collection"><month>12</month><year>2019</year></pub-date><volume>8</volume><issue>12</issue><elocation-id>1597</elocation-id><history><date date-type="received"><day>11</day><month>10</month><year>2019</year></date><date date-type="accepted"><day>03</day><month>12</month><year>2019</year></date></history><permissions><copyright-statement>© 2019 by the authors.</copyright-statement><copyright-year>2019</copyright-year><license license-type="open-access"><license-p>Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (<ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by/4.0/">http://creativecommons.org/licenses/by/4.0/</ext-link>).</license-p></license></permissions><abstract><p>Autophagy, originally found in liver experiments, is a cellular process that degrades damaged organelle or protein aggregation. This process frees cells from various stress states is a cell survival mechanism under stress stimulation. It is now known that dysregulation of autophagy can cause many liver diseases. Therefore, how to properly regulate autophagy is the key to the treatment of liver injury. mechanistic target of rapamycin (mTOR)is the core hub regulating autophagy, which is subject to different upstream signaling pathways to regulate autophagy. This review summarizes three upstream pathways of mTOR: the phosphoinositide 3-kinase (PI3K)/protein kinase (AKT) signaling pathway, the adenosine monophosphate-activated protein kinase (AMPK) signaling pathway, and the rat sarcoma (Ras)/rapidly accelerated fibrosarcoma (Raf)/mitogen-extracellular activated protein kinase kinase (MEK)/ extracellular-signal-regulated kinase (ERK) signaling pathway, specifically explored their role in liver fibrosis, hepatitis B, non-alcoholic fatty liver, liver cancer, hepatic ischemia reperfusion and other liver diseases through the regulation of mTOR-mediated autophagy. Moreover, we also analyzed the crosstalk between these three pathways, aiming to find new targets for the treatment of human liver disease based on autophagy.</p></abstract><kwd-group><kwd>autophagy</kwd><kwd>AKT</kwd><kwd>AMPK</kwd><kwd>ERK</kwd><kwd>liver diseases</kwd><kwd>mTOR</kwd><kwd>MEK</kwd><kwd>PI3K</kwd><kwd>Ras</kwd><kwd>Raf</kwd></kwd-group></article-meta></front><floats-group><fig id="cells-08-01597-f001" orientation="portrait" position="float"><label>Figure 1</label><caption><p>The process and mechanism of autophagy signals that activate the autophagic process (initiation) typically originate from various conditions of stress, such as starvation, hypoxia, oxidative stress, protein aggregation, endoplasmic reticulum (ER) stress and others. The common target of these signaling pathways is the uncoordinated 51-like kinase (ULK) complex (consisting of ULK1/2, ATG13, FIP200 and ATG101) and cause ULK complex translocate to a domain of ER. Upon entry into the ER, the ULK complex initiates nucleation of the phagophore by phosphorylating the class III PI3K complex I (consisting of Beclin-1, PIK3C3/VPS34, PIK3R4/p150, AMBRA1 and ATG14/Barkor). At present, the source of membranes involved in the formation of phagophore remains unclear, possibly ER, mitochondria, Golgi and plasma membrane. After phagophore formation, it will expand and separate damaged organelles (including ER, ribosomes and mitochondria, etc.) and misfolded proteins. As the phagophore expands, the membrane bends, eventually forming a bilayer membrane structure-autophagosome. The ATG12-ATG5-ATg16L1 complex and the LC3-phosphatidylethanolamine (PE) conjugate play an important role during phagophore elongation and closure. Finally, autophagosomes fuse with lysosomes to form autophagosomes and the cargo in autophagosomes is degraded by acid hydrolases in lysosomes. In addition, the nutrients produced by the degradation are released back to the cytoplasm and reused by the cells.</p></caption><graphic xlink:href="cells-08-01597-g001"></graphic></fig><fig id="cells-08-01597-f002" orientation="portrait" position="float"><label>Figure 2</label><caption><p>Overview of mTOR signaling pathway (<bold>A</bold>) The primary structure of mTOR. See text for details. (<bold>B</bold>) Molecular composition and upstream and downstream pathways of mTORC1/2: mTOR kinase forms two distinct protein complexes, called mTORC1 and mTORC2, respectively. (Left) mTORC1 consists of three core components (mTOR, Raptor, mLST8) and two inhibitory subunits (PRAS40, Deptor). (Right) mTORC2 consists of four core components (mTOR, Rictor, mLST8, mSIN1) and one inhibitory subunit Deptor. mTORC1 is regulated by growth factors, energy, oxygen and amino acids and is very sensitive to rapamycin. On the one hand, it promotes anabolism by phosphorylation of its substrates S6K1, 4EBP1 and SREBP to accelerate the synthesis of proteins and lipids, on the other hand, it inhibits catabolism by phosphorylation of ULK complex or other ways to prevent autophagy. mTORC2 responds to growth factors; it regulates cell migration, cytoskeletal remodeling, cell growth and proliferation, ion transport, and cell survival through its downstream substrates PKC, AKT, and SGK1. Moreover, mTORC2 is not sensitive to acute rapamycin treatment, but prolonged exposure to the drug can destroys its structure.</p></caption><graphic xlink:href="cells-08-01597-g002"></graphic></fig><fig id="cells-08-01597-f003" orientation="portrait" position="float"><label>Figure 3</label><caption><p>The upstream pathway of mTOR regulates autophagy. The arrows represent the promotion and the blunt arrows represent the inhibition. P represents phosphorylation. See text for details.</p></caption><graphic xlink:href="cells-08-01597-g003"></graphic></fig><fig id="cells-08-01597-f004" orientation="portrait" position="float"><label>Figure 4</label><caption><p>Adenosine monophosphate-activated protein kinase (AMPK) structure and function AMPK are heterotrimeric proteins comprising a catalytic subunit (α subunit) and two regulatory subunits (β subunit and γ subunit), the domain composition of each subunit being shown. Thr172 is a key site for the activation of AMPK. The upstream kinases LKB1 and CAMKK2 are activated by various metabolic stresses and intracellular calcium, respectively. Activation of LKB1 and CAMKK2 activates AMPK by phosphorylation of Thr172. As an energy-sensing kinase, once activated, AMPK inhibits the energy-consuming synthesis process (that is, adenosine triphosphate (ATP) consumption), such as the biosynthesis of lipids, proteins, and carbohydrates, while simultaneously activating the energy-producing process (that is, ATP production), such as glucose metabolism and autophagy to maintain the balance of energy.</p></caption><graphic xlink:href="cells-08-01597-g004"></graphic></fig><fig id="cells-08-01597-f005" orientation="portrait" position="float"><label>Figure 5</label><caption><p>Cross-talk between PI3K/AKT, AMPK and Ras/Raf/MEK/ERK pathway. Black lines indicate crosstalk between the three pathways, with arrows indicating promotion and blunt arrows indicating inhibition. The blue lines indicate the relationship of the three paths themselves. P represents phosphorylation, -P represents dephosphorylation. See text for details.</p></caption><graphic xlink:href="cells-08-01597-g005"></graphic></fig><fig id="cells-08-01597-f006" orientation="portrait" position="float"><label>Figure 6</label><caption><p>The upstream pathway of mTOR-mediated autophagy in liver injury. PI3K/AKT regulates liver injury by inhibiting mTOR-mediated autophagy. AMPK regulates liver injury by activating mTOR-mediated autophagy. Ras/Raf/MEK/ERK regulates liver injury by inhibiting mTOR-mediated autophagy. PI3K/AKT/mTOR signaling pathway, AMPK/mTOR signaling pathway and Ras/Raf/MEK/ERK/mTOR signaling pathway are emerging targets for drug-based autophagy in the treatment of liver injury.</p></caption><graphic xlink:href="cells-08-01597-g006"></graphic></fig><table-wrap id="cells-08-01597-t001" orientation="portrait" position="float"><object-id pub-id-type="pii">cells-08-01597-t001_Table 1</object-id><label>Table 1</label><caption><p>The role of upstream pathway of mTOR-mediated autophagy in liver disease.</p></caption><table frame="hsides" rules="groups"><thead><tr><th align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">Liver Disease</th><th align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">Signaling Pathway</th><th align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">Effect</th><th align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">Target</th><th align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">Reference</th></tr></thead><tbody><tr><td align="center" valign="middle" rowspan="1" colspan="1">Liver Fibrosis</td><td align="center" valign="middle" rowspan="1" colspan="1">PI3K/AKT/mTOR/autophagy</td><td align="center" valign="middle" rowspan="1" colspan="1">IGFBPrP1 promotes the activation of HSCs by activating PI3K/AKT/mTOR-mediated autophagy.<break></break>MH, Rutin and Curcumin inhibit the activation of HSCs by activating PI3K/AKT/mTOR-mediated autophagy.</td><td align="center" valign="middle" rowspan="1" colspan="1">Inhibition of PI3K/AKT/mTOR-<break></break>mediated autophagy<break></break>Over-activation of PI3K/AKT/<break></break>mTOR-mediated autophagy</td><td align="center" valign="middle" rowspan="1" colspan="1">[<xref rid="B153-cells-08-01597" ref-type="bibr">153</xref>]<break></break>[<xref rid="B154-cells-08-01597" ref-type="bibr">154</xref>,<xref rid="B155-cells-08-01597" ref-type="bibr">155</xref>]</td></tr><tr><td align="center" valign="middle" rowspan="1" colspan="1">Hepatitis B virus</td><td align="center" valign="middle" rowspan="1" colspan="1">PI3K/AKT/mTOR/autophagy</td><td align="center" valign="middle" rowspan="1" colspan="1">microRNA-99 family can promote replication of HBV by inducing PI3K/AKT/mTOR-mediated autophagy.</td><td align="center" valign="middle" rowspan="1" colspan="1">Inhibition of PI3K/AKT/mTOR-<break></break>mediated autophagy</td><td align="center" valign="middle" rowspan="1" colspan="1">[<xref rid="B157-cells-08-01597" ref-type="bibr">157</xref>]</td></tr><tr><td align="center" valign="middle" rowspan="1" colspan="1">Non-alcoholic fatty liver disease</td><td align="center" valign="middle" rowspan="1" colspan="1">AMPK/mTOR/autophagy</td><td align="center" valign="middle" rowspan="1" colspan="1">LRG, FNDC5 and H<sub>2</sub>S activate AMPK/mTOR-mediated autophagy improve NAFLD.<break></break>Acetaminophen inhibits AMPK/mTOR-mediated autophagy aggravating fat accumulation in NAFLD.</td><td align="center" valign="middle" rowspan="1" colspan="1">Activation of AMPK/mTOR-<break></break>mediated autophagy</td><td align="center" valign="middle" rowspan="1" colspan="1">[<xref rid="B201-cells-08-01597" ref-type="bibr">201</xref>,<xref rid="B202-cells-08-01597" ref-type="bibr">202</xref>]<break></break>[<xref rid="B204-cells-08-01597" ref-type="bibr">204</xref>]<break></break>[<xref rid="B207-cells-08-01597" ref-type="bibr">207</xref>] </td></tr><tr><td align="center" valign="middle" rowspan="1" colspan="1">Liver ischemia and reperfusion</td><td align="center" valign="middle" rowspan="1" colspan="1">AMPK/mTOR/autophagy</td><td align="center" valign="middle" rowspan="1" colspan="1">Isoflurane activates AMPK/mTOR pathway mediated autophagy to improve hepatic ischemia-reperfusion injury.<break></break>Inhibition of GSK3β can ameliorate hepatic ischemia-reperfusion injury by activating AMPK/mTOR-mediated autophagy.</td><td align="center" valign="middle" rowspan="1" colspan="1">Activation of AMPK/mTOR-<break></break>mediated autophagy</td><td align="center" valign="middle" rowspan="1" colspan="1">[<xref rid="B108-cells-08-01597" ref-type="bibr">108</xref>]<break></break>[<xref rid="B212-cells-08-01597" ref-type="bibr">212</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Liver Cancer </td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">PI3K/AKT/mTOR/autophagy<break></break>AMPK/mTOR/autophagy<break></break>Ras/Raf/MEK/ERK/<break></break>mTOR/autophagy</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Brusatol activates PI3K/AKT/mTOR-mediated autophagy of hepatoma cells, thereby effectively inducing apoptosis of hepatoma cells, inhibiting proliferation of hepatoma cells as well as invasion and migration of tumors.<break></break>Bri and BCLB over-activate AMPK/mTOR-mediated autophagy to inhibit the growth and proliferation of hepatoma cells.<break></break>Glycochenodeoxycholate activates AMPK/mTOR-mediated autophagy to promote hepatocellular carcinoma invasion and migration.<break></break>RA-XII inhibits AMPK/mTOR-mediated autophagy to inhibit the growth and colony formation of HepG 2 cells.<break></break>Bicyclol and AZA activate Ras/Raf/MEK/ERK/<break></break>mTOR-mediated autophagy to inhibit the proliferation of HepG2 or promote their senescence.</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Over-activation of PI3K/AKT/<break></break>mTOR-mediated autophagy<break></break>Over-activation of AMPK/mTOR-<break></break>mediated autophagy<break></break>Inhibition of AMPK/mTOR-<break></break>mediated autophagy<break></break>Activation of Ras/Raf/MEK/ERK/<break></break>mTOR-mediated autophagy</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B167-cells-08-01597" ref-type="bibr">167</xref>]<break></break>[<xref rid="B214-cells-08-01597" ref-type="bibr">214</xref>,<xref rid="B215-cells-08-01597" ref-type="bibr">215</xref>]<break></break>[<xref rid="B217-cells-08-01597" ref-type="bibr">217</xref>]<break></break>[<xref rid="B109-cells-08-01597" ref-type="bibr">109</xref>]<break></break>[<xref rid="B242-cells-08-01597" ref-type="bibr">242</xref>,<xref rid="B243-cells-08-01597" ref-type="bibr">243</xref>]</td></tr></tbody></table></table-wrap></floats-group></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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