TBC1D25 alleviates nonalcoholic steatohepatitis by inhibiting abnormal lipid accumulation and inflammation
Nonalcoholic fatty liver disease (NAFLD) is a strong stimulant of cardiovascular diseases, affecting one‐quarter of the world's population. TBC1 domain family member 25 (TBC1D25) regulates the development of myocardial hypertrophy and cerebral ischemia–reperfusion injury; however, its effect on...
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| Veröffentlicht in: | Journal of cellular physiology 2023-02, Vol.238 (2), p.393-406 |
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| container_title | Journal of cellular physiology |
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| creator | Wu, Anding Ye, Mao Ma, Tengfei She, Zhigang Li, Ruyan Shi, Hongjie Yang, Ling Yi, Maolin Li, Huoping |
| description | Nonalcoholic fatty liver disease (NAFLD) is a strong stimulant of cardiovascular diseases, affecting one‐quarter of the world's population. TBC1 domain family member 25 (TBC1D25) regulates the development of myocardial hypertrophy and cerebral ischemia–reperfusion injury; however, its effect on NAFLD/nonalcoholic steatohepatitis (NASH) has not been reported. In this study, we demonstrated that TBC1D25 expression is upregulated in NASH. TBC1D25 deficiency aggravated hepatic steatosis, inflammation, and fibrosis in NASH. In vitro tests revealed that TBC1D25 overexpression restrained NASH responses. Subsequent mechanistic validation experiments demonstrated that TBC1D25 interfered with NASH progression by inhibiting abnormal lipid accumulation and inflammation. TBC1D25 deficiency significantly promoted NASH occurrence and development. Therefore, TBC1D25 may potentially be used as a clinical therapeutic target for NASH treatment. |
| doi_str_mv | 10.1002/jcp.30934 |
| format | Article |
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TBC1 domain family member 25 (TBC1D25) regulates the development of myocardial hypertrophy and cerebral ischemia–reperfusion injury; however, its effect on NAFLD/nonalcoholic steatohepatitis (NASH) has not been reported. In this study, we demonstrated that TBC1D25 expression is upregulated in NASH. TBC1D25 deficiency aggravated hepatic steatosis, inflammation, and fibrosis in NASH. In vitro tests revealed that TBC1D25 overexpression restrained NASH responses. Subsequent mechanistic validation experiments demonstrated that TBC1D25 interfered with NASH progression by inhibiting abnormal lipid accumulation and inflammation. TBC1D25 deficiency significantly promoted NASH occurrence and development. Therefore, TBC1D25 may potentially be used as a clinical therapeutic target for NASH treatment.</description><identifier>ISSN: 0021-9541</identifier><identifier>EISSN: 1097-4652</identifier><identifier>DOI: 10.1002/jcp.30934</identifier><identifier>PMID: 36710714</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>Accumulation ; Animals ; Cardiovascular diseases ; Fatty liver ; Fibrosis ; hepatic steatosis ; Hypercholesterolemia - pathology ; Hypertrophy ; In vitro methods and tests ; Inflammation ; Inflammation - pathology ; Ischemia ; Lipids ; Liver - metabolism ; Liver Cirrhosis - pathology ; Liver diseases ; Male ; Mice ; NASH ; Non-alcoholic Fatty Liver Disease - metabolism ; Reperfusion ; Steatosis ; TAK1 ; TBC1D25 ; Therapeutic targets</subject><ispartof>Journal of cellular physiology, 2023-02, Vol.238 (2), p.393-406</ispartof><rights>2023 Wiley Periodicals LLC.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3534-f796e104b26c1248989f791bab47e1bd38c29ba4f56170fdf2fbf45d44b5013d3</citedby><cites>FETCH-LOGICAL-c3534-f796e104b26c1248989f791bab47e1bd38c29ba4f56170fdf2fbf45d44b5013d3</cites><orcidid>0000-0001-8150-5964</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjcp.30934$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjcp.30934$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36710714$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wu, Anding</creatorcontrib><creatorcontrib>Ye, Mao</creatorcontrib><creatorcontrib>Ma, Tengfei</creatorcontrib><creatorcontrib>She, Zhigang</creatorcontrib><creatorcontrib>Li, Ruyan</creatorcontrib><creatorcontrib>Shi, Hongjie</creatorcontrib><creatorcontrib>Yang, Ling</creatorcontrib><creatorcontrib>Yi, Maolin</creatorcontrib><creatorcontrib>Li, Huoping</creatorcontrib><title>TBC1D25 alleviates nonalcoholic steatohepatitis by inhibiting abnormal lipid accumulation and inflammation</title><title>Journal of cellular physiology</title><addtitle>J Cell Physiol</addtitle><description>Nonalcoholic fatty liver disease (NAFLD) is a strong stimulant of cardiovascular diseases, affecting one‐quarter of the world's population. TBC1 domain family member 25 (TBC1D25) regulates the development of myocardial hypertrophy and cerebral ischemia–reperfusion injury; however, its effect on NAFLD/nonalcoholic steatohepatitis (NASH) has not been reported. In this study, we demonstrated that TBC1D25 expression is upregulated in NASH. TBC1D25 deficiency aggravated hepatic steatosis, inflammation, and fibrosis in NASH. In vitro tests revealed that TBC1D25 overexpression restrained NASH responses. Subsequent mechanistic validation experiments demonstrated that TBC1D25 interfered with NASH progression by inhibiting abnormal lipid accumulation and inflammation. TBC1D25 deficiency significantly promoted NASH occurrence and development. Therefore, TBC1D25 may potentially be used as a clinical therapeutic target for NASH treatment.</description><subject>Accumulation</subject><subject>Animals</subject><subject>Cardiovascular diseases</subject><subject>Fatty liver</subject><subject>Fibrosis</subject><subject>hepatic steatosis</subject><subject>Hypercholesterolemia - pathology</subject><subject>Hypertrophy</subject><subject>In vitro methods and tests</subject><subject>Inflammation</subject><subject>Inflammation - pathology</subject><subject>Ischemia</subject><subject>Lipids</subject><subject>Liver - metabolism</subject><subject>Liver Cirrhosis - pathology</subject><subject>Liver diseases</subject><subject>Male</subject><subject>Mice</subject><subject>NASH</subject><subject>Non-alcoholic Fatty Liver Disease - metabolism</subject><subject>Reperfusion</subject><subject>Steatosis</subject><subject>TAK1</subject><subject>TBC1D25</subject><subject>Therapeutic targets</subject><issn>0021-9541</issn><issn>1097-4652</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp10ctOxCAUBmBiNDpeFr6AIXGjiyoUKGWp4z0mutB1AxQcJrTU0mrm7cWZ0YWJK8Lhy58cfgAOMTrDCOXnc92dESQI3QATjATPaMHyTTBJbzgTjOIdsBvjHCEkBCHbYIcUHCOO6QTMXy6n-CpnUHpvPpwcTIRtaKXXYRa80zAORg5hZjo5uMFFqBbQtTOn0qV9g1K1oW-kh951roZS67EZfaKhhbKtE7VeNs1ysA-2rPTRHKzPPfB6c_0yvcsen27vpxePmSaM0MxyURiMqMoLjXNailKkEVZSUW6wqkmpc6EktazAHNna5lZZympKFUOY1GQPnKxyuz68jyYOVeOiNt7L1oQxVjlPy5esLGiix3_oPIx92n6pyoIhzllSpyul-xBjb2zV9a6R_aLCqPouoEoFVMsCkj1aJ46qMfWv_PnxBM5X4NN5s_g_qXqYPq8ivwCMWY-4</recordid><startdate>202302</startdate><enddate>202302</enddate><creator>Wu, Anding</creator><creator>Ye, Mao</creator><creator>Ma, Tengfei</creator><creator>She, Zhigang</creator><creator>Li, Ruyan</creator><creator>Shi, Hongjie</creator><creator>Yang, Ling</creator><creator>Yi, Maolin</creator><creator>Li, Huoping</creator><general>Wiley Subscription Services, Inc</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>7TK</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-8150-5964</orcidid></search><sort><creationdate>202302</creationdate><title>TBC1D25 alleviates nonalcoholic steatohepatitis by inhibiting abnormal lipid accumulation and inflammation</title><author>Wu, Anding ; Ye, Mao ; Ma, Tengfei ; She, Zhigang ; Li, Ruyan ; Shi, Hongjie ; Yang, Ling ; Yi, Maolin ; Li, Huoping</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3534-f796e104b26c1248989f791bab47e1bd38c29ba4f56170fdf2fbf45d44b5013d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Accumulation</topic><topic>Animals</topic><topic>Cardiovascular diseases</topic><topic>Fatty liver</topic><topic>Fibrosis</topic><topic>hepatic steatosis</topic><topic>Hypercholesterolemia - pathology</topic><topic>Hypertrophy</topic><topic>In vitro methods and tests</topic><topic>Inflammation</topic><topic>Inflammation - pathology</topic><topic>Ischemia</topic><topic>Lipids</topic><topic>Liver - metabolism</topic><topic>Liver Cirrhosis - pathology</topic><topic>Liver diseases</topic><topic>Male</topic><topic>Mice</topic><topic>NASH</topic><topic>Non-alcoholic Fatty Liver Disease - metabolism</topic><topic>Reperfusion</topic><topic>Steatosis</topic><topic>TAK1</topic><topic>TBC1D25</topic><topic>Therapeutic targets</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wu, Anding</creatorcontrib><creatorcontrib>Ye, Mao</creatorcontrib><creatorcontrib>Ma, Tengfei</creatorcontrib><creatorcontrib>She, Zhigang</creatorcontrib><creatorcontrib>Li, Ruyan</creatorcontrib><creatorcontrib>Shi, Hongjie</creatorcontrib><creatorcontrib>Yang, Ling</creatorcontrib><creatorcontrib>Yi, Maolin</creatorcontrib><creatorcontrib>Li, Huoping</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of cellular physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wu, Anding</au><au>Ye, Mao</au><au>Ma, Tengfei</au><au>She, Zhigang</au><au>Li, Ruyan</au><au>Shi, Hongjie</au><au>Yang, Ling</au><au>Yi, Maolin</au><au>Li, Huoping</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>TBC1D25 alleviates nonalcoholic steatohepatitis by inhibiting abnormal lipid accumulation and inflammation</atitle><jtitle>Journal of cellular physiology</jtitle><addtitle>J Cell Physiol</addtitle><date>2023-02</date><risdate>2023</risdate><volume>238</volume><issue>2</issue><spage>393</spage><epage>406</epage><pages>393-406</pages><issn>0021-9541</issn><eissn>1097-4652</eissn><abstract>Nonalcoholic fatty liver disease (NAFLD) is a strong stimulant of cardiovascular diseases, affecting one‐quarter of the world's population. TBC1 domain family member 25 (TBC1D25) regulates the development of myocardial hypertrophy and cerebral ischemia–reperfusion injury; however, its effect on NAFLD/nonalcoholic steatohepatitis (NASH) has not been reported. In this study, we demonstrated that TBC1D25 expression is upregulated in NASH. TBC1D25 deficiency aggravated hepatic steatosis, inflammation, and fibrosis in NASH. In vitro tests revealed that TBC1D25 overexpression restrained NASH responses. Subsequent mechanistic validation experiments demonstrated that TBC1D25 interfered with NASH progression by inhibiting abnormal lipid accumulation and inflammation. TBC1D25 deficiency significantly promoted NASH occurrence and development. 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| subjects | Accumulation Animals Cardiovascular diseases Fatty liver Fibrosis hepatic steatosis Hypercholesterolemia - pathology Hypertrophy In vitro methods and tests Inflammation Inflammation - pathology Ischemia Lipids Liver - metabolism Liver Cirrhosis - pathology Liver diseases Male Mice NASH Non-alcoholic Fatty Liver Disease - metabolism Reperfusion Steatosis TAK1 TBC1D25 Therapeutic targets |
| title | TBC1D25 alleviates nonalcoholic steatohepatitis by inhibiting abnormal lipid accumulation and inflammation |
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