The Role of Autophagy and NLRP3 Inflammasome in Liver Fibrosis
Liver fibrosis is an intrinsic repair process of chronic injury with excessive deposition of extracellular matrix. As an early stage of various liver diseases, liver fibrosis is a reversible pathological process. Therefore, if not being controlled in time, liver fibrosis will evolve into cirrhosis,...
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| Veröffentlicht in: | BioMed research international 2020, Vol.2020 (2020), p.1-8 |
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| description | Liver fibrosis is an intrinsic repair process of chronic injury with excessive deposition of extracellular matrix. As an early stage of various liver diseases, liver fibrosis is a reversible pathological process. Therefore, if not being controlled in time, liver fibrosis will evolve into cirrhosis, liver failure, and liver cancer. It has been demonstrated that hepatic stellate cells (HSCs) play a crucial role in the formation of liver fibrosis. In particular, the activation of HSCs is a key step for liver fibrosis. Recent researches have suggested that autophagy and inflammasome have biological effect on HSC activation. Herein, we review current studies about the impact of autophagy and NOD-like receptors containing pyrin domain 3 (NLRP3) inflammasome on liver fibrosis and the underlying mechanisms. |
| doi_str_mv | 10.1155/2020/7269150 |
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As an early stage of various liver diseases, liver fibrosis is a reversible pathological process. Therefore, if not being controlled in time, liver fibrosis will evolve into cirrhosis, liver failure, and liver cancer. It has been demonstrated that hepatic stellate cells (HSCs) play a crucial role in the formation of liver fibrosis. In particular, the activation of HSCs is a key step for liver fibrosis. Recent researches have suggested that autophagy and inflammasome have biological effect on HSC activation. Herein, we review current studies about the impact of autophagy and NOD-like receptors containing pyrin domain 3 (NLRP3) inflammasome on liver fibrosis and the underlying mechanisms.</description><identifier>ISSN: 2314-6133</identifier><identifier>EISSN: 2314-6141</identifier><identifier>DOI: 10.1155/2020/7269150</identifier><identifier>PMID: 32733951</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Activation ; Animals ; Autophagy ; Autophagy (Cytology) ; Bile ; Binding sites ; Biological effects ; Chemokines ; Cirrhosis ; Cytokines ; Extracellular matrix ; Fibrosis ; Free radicals ; Growth factors ; Health aspects ; Hepatic Stellate Cells - pathology ; Hepatitis ; Humans ; Inflammasomes ; Inflammasomes - metabolism ; Inflammation ; Kinases ; Liver ; Liver cancer ; Liver cirrhosis ; Liver Cirrhosis - metabolism ; Liver Cirrhosis - pathology ; Liver diseases ; NLR Family, Pyrin Domain-Containing 3 Protein - metabolism ; Oxidative Stress ; Phagocytosis ; Physiological aspects ; Proteins ; Pyrin protein ; Review ; Stellate cells ; Tumor necrosis factor-TNF</subject><ispartof>BioMed research international, 2020, Vol.2020 (2020), p.1-8</ispartof><rights>Copyright © 2020 Ye Tao et al.</rights><rights>COPYRIGHT 2020 John Wiley & Sons, Inc.</rights><rights>Copyright © 2020 Ye Tao et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. http://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2020 Ye Tao et al. 2020</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c499t-506d82400445cda07c02e1dec696fae536a85fb79683cdfe74bdfa1c35c3ae5e3</citedby><cites>FETCH-LOGICAL-c499t-506d82400445cda07c02e1dec696fae536a85fb79683cdfe74bdfa1c35c3ae5e3</cites><orcidid>0000-0003-1203-071X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7369671/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7369671/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,4010,27900,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32733951$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Minor, Thomas</contributor><creatorcontrib>Sun, Xiance</creatorcontrib><creatorcontrib>Qiu, Tianming</creatorcontrib><creatorcontrib>Wang, Ningning</creatorcontrib><creatorcontrib>Tao, Ye</creatorcontrib><title>The Role of Autophagy and NLRP3 Inflammasome in Liver Fibrosis</title><title>BioMed research international</title><addtitle>Biomed Res Int</addtitle><description>Liver fibrosis is an intrinsic repair process of chronic injury with excessive deposition of extracellular matrix. As an early stage of various liver diseases, liver fibrosis is a reversible pathological process. Therefore, if not being controlled in time, liver fibrosis will evolve into cirrhosis, liver failure, and liver cancer. It has been demonstrated that hepatic stellate cells (HSCs) play a crucial role in the formation of liver fibrosis. In particular, the activation of HSCs is a key step for liver fibrosis. Recent researches have suggested that autophagy and inflammasome have biological effect on HSC activation. Herein, we review current studies about the impact of autophagy and NOD-like receptors containing pyrin domain 3 (NLRP3) inflammasome on liver fibrosis and the underlying mechanisms.</description><subject>Activation</subject><subject>Animals</subject><subject>Autophagy</subject><subject>Autophagy (Cytology)</subject><subject>Bile</subject><subject>Binding sites</subject><subject>Biological effects</subject><subject>Chemokines</subject><subject>Cirrhosis</subject><subject>Cytokines</subject><subject>Extracellular matrix</subject><subject>Fibrosis</subject><subject>Free radicals</subject><subject>Growth factors</subject><subject>Health aspects</subject><subject>Hepatic Stellate Cells - pathology</subject><subject>Hepatitis</subject><subject>Humans</subject><subject>Inflammasomes</subject><subject>Inflammasomes - metabolism</subject><subject>Inflammation</subject><subject>Kinases</subject><subject>Liver</subject><subject>Liver cancer</subject><subject>Liver cirrhosis</subject><subject>Liver Cirrhosis - metabolism</subject><subject>Liver Cirrhosis - pathology</subject><subject>Liver diseases</subject><subject>NLR Family, Pyrin Domain-Containing 3 Protein - metabolism</subject><subject>Oxidative Stress</subject><subject>Phagocytosis</subject><subject>Physiological aspects</subject><subject>Proteins</subject><subject>Pyrin protein</subject><subject>Review</subject><subject>Stellate cells</subject><subject>Tumor necrosis factor-TNF</subject><issn>2314-6133</issn><issn>2314-6141</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqNkc1LIzEYh4PsYsX1tuclsMe1mu9MLkIRv6CsIt1zSDNv2pSZSZ20iv-9kdZWb5tLAu_Dk1_yQ-gnJWeUSnnOCCPnmilDJTlAR4xTMVRU0G-7M-cDdJLzgpRVUUWMOkQDzjTnRtIjdDGZA35MDeAU8Gi9Ssu5m71i19X47_jxgeO7LjSubV1OLeDY4XF8hh5fx2mfcsw_0Pfgmgwn2_0Y_bu-mlzeDsf3N3eXo_HQC2NWQ0lUXTFBiBDS145oTxjQGrwyKjiQXLlKhqk2quK-DqDFtA6Oei49L2Pgx-hi412upy3UHrpV7xq77GPr-lebXLRfJ12c21l6tpqXKzQtgt9bQZ-e1pBXdpHWfVcyWyaYqHQlFNtTM9eAjV1IRebbmL0dKW6qihBtCnW6oXz5g9xD2OWgxL7XYt9rsdtaCv7rc_Yd_FFCAf5sgHnsavcS_1MHhYHg9jTl5aWEvwGqVpxl</recordid><startdate>2020</startdate><enddate>2020</enddate><creator>Sun, Xiance</creator><creator>Qiu, Tianming</creator><creator>Wang, Ningning</creator><creator>Tao, Ye</creator><general>Hindawi Publishing Corporation</general><general>Hindawi</general><general>John Wiley & Sons, Inc</general><general>Hindawi Limited</general><scope>ADJCN</scope><scope>AHFXO</scope><scope>RHU</scope><scope>RHW</scope><scope>RHX</scope><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>3V.</scope><scope>7QL</scope><scope>7QO</scope><scope>7T7</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>CWDGH</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-1203-071X</orcidid></search><sort><creationdate>2020</creationdate><title>The Role of Autophagy and NLRP3 Inflammasome in Liver Fibrosis</title><author>Sun, Xiance ; Qiu, Tianming ; Wang, Ningning ; Tao, Ye</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c499t-506d82400445cda07c02e1dec696fae536a85fb79683cdfe74bdfa1c35c3ae5e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Activation</topic><topic>Animals</topic><topic>Autophagy</topic><topic>Autophagy (Cytology)</topic><topic>Bile</topic><topic>Binding sites</topic><topic>Biological effects</topic><topic>Chemokines</topic><topic>Cirrhosis</topic><topic>Cytokines</topic><topic>Extracellular matrix</topic><topic>Fibrosis</topic><topic>Free radicals</topic><topic>Growth factors</topic><topic>Health aspects</topic><topic>Hepatic Stellate Cells - pathology</topic><topic>Hepatitis</topic><topic>Humans</topic><topic>Inflammasomes</topic><topic>Inflammasomes - metabolism</topic><topic>Inflammation</topic><topic>Kinases</topic><topic>Liver</topic><topic>Liver cancer</topic><topic>Liver cirrhosis</topic><topic>Liver Cirrhosis - metabolism</topic><topic>Liver Cirrhosis - pathology</topic><topic>Liver diseases</topic><topic>NLR Family, Pyrin Domain-Containing 3 Protein - metabolism</topic><topic>Oxidative Stress</topic><topic>Phagocytosis</topic><topic>Physiological aspects</topic><topic>Proteins</topic><topic>Pyrin protein</topic><topic>Review</topic><topic>Stellate cells</topic><topic>Tumor necrosis factor-TNF</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sun, Xiance</creatorcontrib><creatorcontrib>Qiu, Tianming</creatorcontrib><creatorcontrib>Wang, Ningning</creatorcontrib><creatorcontrib>Tao, Ye</creatorcontrib><collection>الدوريات العلمية والإحصائية - e-Marefa Academic and Statistical Periodicals</collection><collection>معرفة - 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As an early stage of various liver diseases, liver fibrosis is a reversible pathological process. Therefore, if not being controlled in time, liver fibrosis will evolve into cirrhosis, liver failure, and liver cancer. It has been demonstrated that hepatic stellate cells (HSCs) play a crucial role in the formation of liver fibrosis. In particular, the activation of HSCs is a key step for liver fibrosis. Recent researches have suggested that autophagy and inflammasome have biological effect on HSC activation. Herein, we review current studies about the impact of autophagy and NOD-like receptors containing pyrin domain 3 (NLRP3) inflammasome on liver fibrosis and the underlying mechanisms.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>32733951</pmid><doi>10.1155/2020/7269150</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0003-1203-071X</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Activation Animals Autophagy Autophagy (Cytology) Bile Binding sites Biological effects Chemokines Cirrhosis Cytokines Extracellular matrix Fibrosis Free radicals Growth factors Health aspects Hepatic Stellate Cells - pathology Hepatitis Humans Inflammasomes Inflammasomes - metabolism Inflammation Kinases Liver Liver cancer Liver cirrhosis Liver Cirrhosis - metabolism Liver Cirrhosis - pathology Liver diseases NLR Family, Pyrin Domain-Containing 3 Protein - metabolism Oxidative Stress Phagocytosis Physiological aspects Proteins Pyrin protein Review Stellate cells Tumor necrosis factor-TNF |
| title | The Role of Autophagy and NLRP3 Inflammasome in Liver Fibrosis |
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