The Upstream Pathway of mTOR-Mediated Autophagy in Liver Diseases
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 li...
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| Veröffentlicht in: | Cells (Basel, Switzerland) Switzerland), 2019-12, Vol.8 (12), p.1597 |
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| creator | Wang, Haojie Liu, Yumei Wang, Dongmei Xu, Yaolu Dong, Ruiqi Yang, Yuxiang Lv, Qiongxia Chen, Xiaoguang Zhang, Ziqiang |
| description | 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. |
| doi_str_mv | 10.3390/cells8121597 |
| format | Article |
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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.</description><identifier>ISSN: 2073-4409</identifier><identifier>EISSN: 2073-4409</identifier><identifier>DOI: 10.3390/cells8121597</identifier><identifier>PMID: 31835352</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>1-Phosphatidylinositol 3-kinase ; Adenosine kinase ; AKT protein ; AMP ; Animals ; Apoptosis ; Autophagy ; Autophagy - genetics ; Autophagy - physiology ; Cell survival ; Endoplasmic reticulum ; Enzymes ; Extracellular signal-regulated kinase ; Extracellular Signal-Regulated MAP Kinases - genetics ; Extracellular Signal-Regulated MAP Kinases - metabolism ; Fatty liver ; Fibrosarcoma ; Fibrosis ; Hepatitis B ; Hepatocytes ; Humans ; Ischemia ; Kinases ; Liver cancer ; Liver diseases ; Liver Diseases - genetics ; Liver Diseases - metabolism ; Lymphoma ; Membranes ; Metabolism ; Mitochondria ; Mitogen-Activated Protein Kinase Kinases - genetics ; Mitogen-Activated Protein Kinase Kinases - metabolism ; Phagocytosis ; Phosphatidylinositol 3-Kinases - genetics ; Phosphatidylinositol 3-Kinases - metabolism ; Protein interaction ; Protein kinase ; Proteins ; Raf protein ; Rapamycin ; Reperfusion ; Review ; Signal transduction ; Signal Transduction - genetics ; Signal Transduction - physiology ; TOR protein</subject><ispartof>Cells (Basel, Switzerland), 2019-12, Vol.8 (12), p.1597</ispartof><rights>2019 by the authors. 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 (http://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2019 by the authors. 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c478t-4213a9759f51cfd977a5c46dc3805e9c0262b6ff4d55825e3d88eea67f4d60df3</citedby><cites>FETCH-LOGICAL-c478t-4213a9759f51cfd977a5c46dc3805e9c0262b6ff4d55825e3d88eea67f4d60df3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6953127/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6953127/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,724,777,781,861,882,27905,27906,53772,53774</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31835352$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Haojie</creatorcontrib><creatorcontrib>Liu, Yumei</creatorcontrib><creatorcontrib>Wang, Dongmei</creatorcontrib><creatorcontrib>Xu, Yaolu</creatorcontrib><creatorcontrib>Dong, Ruiqi</creatorcontrib><creatorcontrib>Yang, Yuxiang</creatorcontrib><creatorcontrib>Lv, Qiongxia</creatorcontrib><creatorcontrib>Chen, Xiaoguang</creatorcontrib><creatorcontrib>Zhang, Ziqiang</creatorcontrib><title>The Upstream Pathway of mTOR-Mediated Autophagy in Liver Diseases</title><title>Cells (Basel, Switzerland)</title><addtitle>Cells</addtitle><description>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.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>Adenosine kinase</subject><subject>AKT protein</subject><subject>AMP</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Autophagy</subject><subject>Autophagy - genetics</subject><subject>Autophagy - physiology</subject><subject>Cell survival</subject><subject>Endoplasmic reticulum</subject><subject>Enzymes</subject><subject>Extracellular signal-regulated kinase</subject><subject>Extracellular Signal-Regulated MAP Kinases - genetics</subject><subject>Extracellular Signal-Regulated MAP Kinases - metabolism</subject><subject>Fatty liver</subject><subject>Fibrosarcoma</subject><subject>Fibrosis</subject><subject>Hepatitis B</subject><subject>Hepatocytes</subject><subject>Humans</subject><subject>Ischemia</subject><subject>Kinases</subject><subject>Liver cancer</subject><subject>Liver diseases</subject><subject>Liver Diseases - genetics</subject><subject>Liver Diseases - metabolism</subject><subject>Lymphoma</subject><subject>Membranes</subject><subject>Metabolism</subject><subject>Mitochondria</subject><subject>Mitogen-Activated Protein Kinase Kinases - genetics</subject><subject>Mitogen-Activated Protein Kinase Kinases - metabolism</subject><subject>Phagocytosis</subject><subject>Phosphatidylinositol 3-Kinases - genetics</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Protein interaction</subject><subject>Protein kinase</subject><subject>Proteins</subject><subject>Raf protein</subject><subject>Rapamycin</subject><subject>Reperfusion</subject><subject>Review</subject><subject>Signal transduction</subject><subject>Signal Transduction - genetics</subject><subject>Signal Transduction - physiology</subject><subject>TOR protein</subject><issn>2073-4409</issn><issn>2073-4409</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNpdkctLw0AQxhdRbKm9eZYFLx6M7iOb3VyEUp9QqUh7XrbJpEnJy92k0v_elNZSncsMMz8-ZuZD6JKSO85Dch9BnjtFGRWhPEF9RiT3fJ-Ep0d1Dw2dW5EuFA0oEeeox6niggvWR6NZCnheu8aCKfCHadJvs8FVgovZ9NN7hzgzDcR41DZVnZrlBmclnmRrsPgxc2AcuAt0lpjcwXCfB2j-_DQbv3qT6cvbeDTxIl-qxvMZ5SaUIkwEjZI4lNKIyA_iiCsiIIwIC9giSBI_FkIxATxWCsAEsusEJE74AD3sdOt2UUAcQdlYk-vaZoWxG12ZTP-dlFmql9VaB6HglMlO4GYvYKuvFlyji8xtH2hKqFqnGeeSEOoT2qHX_9BV1dqyO08z4SvOBZWqo253VGQr5ywkh2Uo0Vt79LE9HX51fMAB_jWD_wAoWIqh</recordid><startdate>20191209</startdate><enddate>20191209</enddate><creator>Wang, Haojie</creator><creator>Liu, Yumei</creator><creator>Wang, Dongmei</creator><creator>Xu, Yaolu</creator><creator>Dong, Ruiqi</creator><creator>Yang, Yuxiang</creator><creator>Lv, Qiongxia</creator><creator>Chen, Xiaoguang</creator><creator>Zhang, Ziqiang</creator><general>MDPI AG</general><general>MDPI</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20191209</creationdate><title>The Upstream Pathway of mTOR-Mediated Autophagy in Liver Diseases</title><author>Wang, Haojie ; Liu, Yumei ; Wang, Dongmei ; Xu, Yaolu ; Dong, Ruiqi ; Yang, Yuxiang ; Lv, Qiongxia ; Chen, Xiaoguang ; Zhang, Ziqiang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c478t-4213a9759f51cfd977a5c46dc3805e9c0262b6ff4d55825e3d88eea67f4d60df3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>Adenosine kinase</topic><topic>AKT protein</topic><topic>AMP</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Autophagy</topic><topic>Autophagy - genetics</topic><topic>Autophagy - physiology</topic><topic>Cell survival</topic><topic>Endoplasmic reticulum</topic><topic>Enzymes</topic><topic>Extracellular signal-regulated kinase</topic><topic>Extracellular Signal-Regulated MAP Kinases - genetics</topic><topic>Extracellular Signal-Regulated MAP Kinases - metabolism</topic><topic>Fatty liver</topic><topic>Fibrosarcoma</topic><topic>Fibrosis</topic><topic>Hepatitis B</topic><topic>Hepatocytes</topic><topic>Humans</topic><topic>Ischemia</topic><topic>Kinases</topic><topic>Liver cancer</topic><topic>Liver diseases</topic><topic>Liver Diseases - genetics</topic><topic>Liver Diseases - metabolism</topic><topic>Lymphoma</topic><topic>Membranes</topic><topic>Metabolism</topic><topic>Mitochondria</topic><topic>Mitogen-Activated Protein Kinase Kinases - genetics</topic><topic>Mitogen-Activated Protein Kinase Kinases - metabolism</topic><topic>Phagocytosis</topic><topic>Phosphatidylinositol 3-Kinases - genetics</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Protein interaction</topic><topic>Protein kinase</topic><topic>Proteins</topic><topic>Raf protein</topic><topic>Rapamycin</topic><topic>Reperfusion</topic><topic>Review</topic><topic>Signal transduction</topic><topic>Signal Transduction - genetics</topic><topic>Signal Transduction - physiology</topic><topic>TOR protein</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Haojie</creatorcontrib><creatorcontrib>Liu, Yumei</creatorcontrib><creatorcontrib>Wang, Dongmei</creatorcontrib><creatorcontrib>Xu, Yaolu</creatorcontrib><creatorcontrib>Dong, Ruiqi</creatorcontrib><creatorcontrib>Yang, Yuxiang</creatorcontrib><creatorcontrib>Lv, Qiongxia</creatorcontrib><creatorcontrib>Chen, Xiaoguang</creatorcontrib><creatorcontrib>Zhang, Ziqiang</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cells (Basel, Switzerland)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Haojie</au><au>Liu, Yumei</au><au>Wang, Dongmei</au><au>Xu, Yaolu</au><au>Dong, Ruiqi</au><au>Yang, Yuxiang</au><au>Lv, Qiongxia</au><au>Chen, Xiaoguang</au><au>Zhang, Ziqiang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Upstream Pathway of mTOR-Mediated Autophagy in Liver Diseases</atitle><jtitle>Cells (Basel, Switzerland)</jtitle><addtitle>Cells</addtitle><date>2019-12-09</date><risdate>2019</risdate><volume>8</volume><issue>12</issue><spage>1597</spage><pages>1597-</pages><issn>2073-4409</issn><eissn>2073-4409</eissn><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.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>31835352</pmid><doi>10.3390/cells8121597</doi><oa>free_for_read</oa></addata></record> |
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| subjects | 1-Phosphatidylinositol 3-kinase Adenosine kinase AKT protein AMP Animals Apoptosis Autophagy Autophagy - genetics Autophagy - physiology Cell survival Endoplasmic reticulum Enzymes Extracellular signal-regulated kinase Extracellular Signal-Regulated MAP Kinases - genetics Extracellular Signal-Regulated MAP Kinases - metabolism Fatty liver Fibrosarcoma Fibrosis Hepatitis B Hepatocytes Humans Ischemia Kinases Liver cancer Liver diseases Liver Diseases - genetics Liver Diseases - metabolism Lymphoma Membranes Metabolism Mitochondria Mitogen-Activated Protein Kinase Kinases - genetics Mitogen-Activated Protein Kinase Kinases - metabolism Phagocytosis Phosphatidylinositol 3-Kinases - genetics Phosphatidylinositol 3-Kinases - metabolism Protein interaction Protein kinase Proteins Raf protein Rapamycin Reperfusion Review Signal transduction Signal Transduction - genetics Signal Transduction - physiology TOR protein |
| title | The Upstream Pathway of mTOR-Mediated Autophagy in Liver Diseases |
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