CRISPR/dCas9 for hepatic fibrosis therapy: implications and challenges
Hepatic fibrosis is a pathological reaction of tissue damage and repair caused by various pathogenic factors acting on liver. At present, there is no effective anti-fibrotic specific therapy. Clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 (dCas9) syste...
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| Veröffentlicht in: | Molecular biology reports 2022-12, Vol.49 (12), p.11403-11408 |
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| creator | Luo, Nianan Zhong, Wenjun Li, Jiangbin Lu, Jianguo Dong, Rui |
| description | Hepatic fibrosis is a pathological reaction of tissue damage and repair caused by various pathogenic factors acting on liver. At present, there is no effective anti-fibrotic specific therapy. Clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 (dCas9) system is a new generation of gene editing technology. The CRISPR/dCas9 system provides a platform for studying site-specific transcriptional regulation, which has high efficiency in gene transcriptional activation for achieving robust. This system holds promise for hepatic fibrosis therapy via acting on liver fibrosis effector cells. However, there are some challenges associated with this novel technology, such as large structural variants at on-target, off-target sites, and targeted delivery efficiency. In this review, we present the potential implications and describe the challenges of CRISPR/dCas9 system that might be encountered in hepatic fibrosis therapy. |
| doi_str_mv | 10.1007/s11033-022-07713-6 |
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At present, there is no effective anti-fibrotic specific therapy. Clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 (dCas9) system is a new generation of gene editing technology. The CRISPR/dCas9 system provides a platform for studying site-specific transcriptional regulation, which has high efficiency in gene transcriptional activation for achieving robust. This system holds promise for hepatic fibrosis therapy via acting on liver fibrosis effector cells. However, there are some challenges associated with this novel technology, such as large structural variants at on-target, off-target sites, and targeted delivery efficiency. In this review, we present the potential implications and describe the challenges of CRISPR/dCas9 system that might be encountered in hepatic fibrosis therapy.</description><identifier>ISSN: 0301-4851</identifier><identifier>EISSN: 1573-4978</identifier><identifier>DOI: 10.1007/s11033-022-07713-6</identifier><language>eng</language><publisher>Dordrecht: Springer Netherlands</publisher><subject>Animal Anatomy ; Animal Biochemistry ; Biomedical and Life Sciences ; Biomedical research ; CRISPR ; DNA methylation ; Effector cells ; Fibrosis ; Gene regulation ; Gene therapy ; genes ; Genome editing ; Genomes ; Hepatitis ; Hepatocytes ; Histology ; Homeostasis ; Life Sciences ; Liver ; liver cirrhosis ; Liver diseases ; Molecular biology ; Morphology ; Mouse models and CRISPR technologies – the state of the art ; Mutation ; Original Article ; Proteins ; Signal transduction ; technology ; therapeutics ; transcription (genetics) ; Transcription activation ; Transcription factors ; transcriptional activation</subject><ispartof>Molecular biology reports, 2022-12, Vol.49 (12), p.11403-11408</ispartof><rights>The Author(s), under exclusive licence to Springer Nature B.V. 2022</rights><rights>The Author(s), under exclusive licence to Springer Nature B.V. 2022.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c385t-b6c6b6cb6dd62db98b8fcaab64dbcb71d81a4af4f87c01f4c082e2a021f5ae9c3</citedby><cites>FETCH-LOGICAL-c385t-b6c6b6cb6dd62db98b8fcaab64dbcb71d81a4af4f87c01f4c082e2a021f5ae9c3</cites><orcidid>0000-0002-8642-0238</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11033-022-07713-6$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11033-022-07713-6$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,778,782,27913,27914,41477,42546,51308</link.rule.ids></links><search><creatorcontrib>Luo, Nianan</creatorcontrib><creatorcontrib>Zhong, Wenjun</creatorcontrib><creatorcontrib>Li, Jiangbin</creatorcontrib><creatorcontrib>Lu, Jianguo</creatorcontrib><creatorcontrib>Dong, Rui</creatorcontrib><title>CRISPR/dCas9 for hepatic fibrosis therapy: implications and challenges</title><title>Molecular biology reports</title><addtitle>Mol Biol Rep</addtitle><description>Hepatic fibrosis is a pathological reaction of tissue damage and repair caused by various pathogenic factors acting on liver. At present, there is no effective anti-fibrotic specific therapy. Clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 (dCas9) system is a new generation of gene editing technology. The CRISPR/dCas9 system provides a platform for studying site-specific transcriptional regulation, which has high efficiency in gene transcriptional activation for achieving robust. This system holds promise for hepatic fibrosis therapy via acting on liver fibrosis effector cells. However, there are some challenges associated with this novel technology, such as large structural variants at on-target, off-target sites, and targeted delivery efficiency. 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Zhong, Wenjun ; Li, Jiangbin ; Lu, Jianguo ; Dong, Rui</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c385t-b6c6b6cb6dd62db98b8fcaab64dbcb71d81a4af4f87c01f4c082e2a021f5ae9c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Animal Anatomy</topic><topic>Animal Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedical research</topic><topic>CRISPR</topic><topic>DNA methylation</topic><topic>Effector cells</topic><topic>Fibrosis</topic><topic>Gene regulation</topic><topic>Gene therapy</topic><topic>genes</topic><topic>Genome editing</topic><topic>Genomes</topic><topic>Hepatitis</topic><topic>Hepatocytes</topic><topic>Histology</topic><topic>Homeostasis</topic><topic>Life Sciences</topic><topic>Liver</topic><topic>liver cirrhosis</topic><topic>Liver diseases</topic><topic>Molecular biology</topic><topic>Morphology</topic><topic>Mouse models and CRISPR technologies – the state of the art</topic><topic>Mutation</topic><topic>Original Article</topic><topic>Proteins</topic><topic>Signal transduction</topic><topic>technology</topic><topic>therapeutics</topic><topic>transcription (genetics)</topic><topic>Transcription activation</topic><topic>Transcription factors</topic><topic>transcriptional activation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Luo, Nianan</creatorcontrib><creatorcontrib>Zhong, Wenjun</creatorcontrib><creatorcontrib>Li, Jiangbin</creatorcontrib><creatorcontrib>Lu, Jianguo</creatorcontrib><creatorcontrib>Dong, Rui</creatorcontrib><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</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>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</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>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>AGRICOLA</collection><collection>AGRICOLA - Academic</collection><jtitle>Molecular biology reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Luo, Nianan</au><au>Zhong, Wenjun</au><au>Li, Jiangbin</au><au>Lu, Jianguo</au><au>Dong, Rui</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CRISPR/dCas9 for hepatic fibrosis therapy: implications and challenges</atitle><jtitle>Molecular biology reports</jtitle><stitle>Mol Biol Rep</stitle><date>2022-12-01</date><risdate>2022</risdate><volume>49</volume><issue>12</issue><spage>11403</spage><epage>11408</epage><pages>11403-11408</pages><issn>0301-4851</issn><eissn>1573-4978</eissn><abstract>Hepatic fibrosis is a pathological reaction of tissue damage and repair caused by various pathogenic factors acting on liver. At present, there is no effective anti-fibrotic specific therapy. Clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 (dCas9) system is a new generation of gene editing technology. The CRISPR/dCas9 system provides a platform for studying site-specific transcriptional regulation, which has high efficiency in gene transcriptional activation for achieving robust. This system holds promise for hepatic fibrosis therapy via acting on liver fibrosis effector cells. However, there are some challenges associated with this novel technology, such as large structural variants at on-target, off-target sites, and targeted delivery efficiency. In this review, we present the potential implications and describe the challenges of CRISPR/dCas9 system that might be encountered in hepatic fibrosis therapy.</abstract><cop>Dordrecht</cop><pub>Springer Netherlands</pub><doi>10.1007/s11033-022-07713-6</doi><tpages>6</tpages><orcidid>https://orcid.org/0000-0002-8642-0238</orcidid></addata></record> |
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| subjects | Animal Anatomy Animal Biochemistry Biomedical and Life Sciences Biomedical research CRISPR DNA methylation Effector cells Fibrosis Gene regulation Gene therapy genes Genome editing Genomes Hepatitis Hepatocytes Histology Homeostasis Life Sciences Liver liver cirrhosis Liver diseases Molecular biology Morphology Mouse models and CRISPR technologies – the state of the art Mutation Original Article Proteins Signal transduction technology therapeutics transcription (genetics) Transcription activation Transcription factors transcriptional activation |
| title | CRISPR/dCas9 for hepatic fibrosis therapy: implications and challenges |
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