Celastrol suppresses lipid accumulation through LXRα/ABCA1 signaling pathway and autophagy in vascular smooth muscle cells
The uptake of modified low-density lipoprotein (LDL) and the accumulation of lipid droplets induce the formation of vascular smooth muscle cells (VSMCs)-derived foam cells, thereby promoting the development and maturation of plaques and accelerating the progression of atherosclerosis. Celastrol is a...
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| Veröffentlicht in: | Biochemical and biophysical research communications 2020-11, Vol.532 (3), p.466-474 |
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| creator | Shi, Yaning Jiang, Shuang Zhao, Tanjun Gong, Yongzhen Liao, Duanfang Qin, Li |
| description | The uptake of modified low-density lipoprotein (LDL) and the accumulation of lipid droplets induce the formation of vascular smooth muscle cells (VSMCs)-derived foam cells, thereby promoting the development and maturation of plaques and accelerating the progression of atherosclerosis. Celastrol is a quinine methide triterpenoid isolated from the root bark of traditional Chinese herb Tripterygium wilfordii. It possesses various biological properties, including anti-obesity, cardiovascular protection, anti-inflammation, etc. In the present study, we found that celastrol significantly reduced lipid accumulation induced by oxidized LDL (ox-LDL) in VSMCs. Mechanistically, celastrol up-regulated adenosine triphosphate-binding cassette transporter A1 (ABCA1) expression through activating liver X receptor α (LXRα) expression, which contributed to inhibit lipid accumulation in VSMCs. Meanwhile, celastrol decreased lipid accumulation by triggering autophagy in VSMCs. Therefore, these findings supported celastrol as a potentially effective agent for the prevention and therapy of atherosclerosis.
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•Celastrol suppresses lipid accumulation by activating LXRα/ABCA1 signaling in VSMCs.•Celastrol inhibits lipid storage by inducing autophagy in VSMCs.•Celastrol is a potentially effective agent for treatment of atherosclerosis. |
| doi_str_mv | 10.1016/j.bbrc.2020.08.076 |
| format | Article |
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•Celastrol suppresses lipid accumulation by activating LXRα/ABCA1 signaling in VSMCs.•Celastrol inhibits lipid storage by inducing autophagy in VSMCs.•Celastrol is a potentially effective agent for treatment of atherosclerosis.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1016/j.bbrc.2020.08.076</identifier><identifier>PMID: 32892949</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Atherosclerosis ; Atherosclerosis - drug therapy ; Atherosclerosis - metabolism ; Atherosclerosis - prevention & control ; ATP Binding Cassette Transporter 1 - metabolism ; Autophagy ; Autophagy - drug effects ; Celastrol ; Cells, Cultured ; Foam Cells - drug effects ; Foam Cells - metabolism ; Foam Cells - pathology ; Humans ; Lipid accumulation ; Lipid Metabolism - drug effects ; Lipoproteins, LDL - metabolism ; Lipoproteins, LDL - pharmacology ; Liver X Receptors - metabolism ; LXRα/ABCA1 signaling pathway ; Muscle, Smooth, Vascular - cytology ; Muscle, Smooth, Vascular - drug effects ; Muscle, Smooth, Vascular - metabolism ; Myocytes, Smooth Muscle - cytology ; Myocytes, Smooth Muscle - drug effects ; Myocytes, Smooth Muscle - metabolism ; Signal Transduction - drug effects ; Triterpenes - pharmacology ; Vascular smooth muscle cells</subject><ispartof>Biochemical and biophysical research communications, 2020-11, Vol.532 (3), p.466-474</ispartof><rights>2020 Elsevier Inc.</rights><rights>Copyright © 2020 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c356t-1c3b7661c82499170773402f4feec23c1d6912bce22fb024bf24fcca548e3093</citedby><cites>FETCH-LOGICAL-c356t-1c3b7661c82499170773402f4feec23c1d6912bce22fb024bf24fcca548e3093</cites><orcidid>0000-0002-9797-2636</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.bbrc.2020.08.076$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,777,781,3537,27905,27906,45976</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32892949$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shi, Yaning</creatorcontrib><creatorcontrib>Jiang, Shuang</creatorcontrib><creatorcontrib>Zhao, Tanjun</creatorcontrib><creatorcontrib>Gong, Yongzhen</creatorcontrib><creatorcontrib>Liao, Duanfang</creatorcontrib><creatorcontrib>Qin, Li</creatorcontrib><title>Celastrol suppresses lipid accumulation through LXRα/ABCA1 signaling pathway and autophagy in vascular smooth muscle cells</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>The uptake of modified low-density lipoprotein (LDL) and the accumulation of lipid droplets induce the formation of vascular smooth muscle cells (VSMCs)-derived foam cells, thereby promoting the development and maturation of plaques and accelerating the progression of atherosclerosis. Celastrol is a quinine methide triterpenoid isolated from the root bark of traditional Chinese herb Tripterygium wilfordii. It possesses various biological properties, including anti-obesity, cardiovascular protection, anti-inflammation, etc. In the present study, we found that celastrol significantly reduced lipid accumulation induced by oxidized LDL (ox-LDL) in VSMCs. Mechanistically, celastrol up-regulated adenosine triphosphate-binding cassette transporter A1 (ABCA1) expression through activating liver X receptor α (LXRα) expression, which contributed to inhibit lipid accumulation in VSMCs. Meanwhile, celastrol decreased lipid accumulation by triggering autophagy in VSMCs. Therefore, these findings supported celastrol as a potentially effective agent for the prevention and therapy of atherosclerosis.
[Display omitted]
•Celastrol suppresses lipid accumulation by activating LXRα/ABCA1 signaling in VSMCs.•Celastrol inhibits lipid storage by inducing autophagy in VSMCs.•Celastrol is a potentially effective agent for treatment of atherosclerosis.</description><subject>Atherosclerosis</subject><subject>Atherosclerosis - drug therapy</subject><subject>Atherosclerosis - metabolism</subject><subject>Atherosclerosis - prevention & control</subject><subject>ATP Binding Cassette Transporter 1 - metabolism</subject><subject>Autophagy</subject><subject>Autophagy - drug effects</subject><subject>Celastrol</subject><subject>Cells, Cultured</subject><subject>Foam Cells - drug effects</subject><subject>Foam Cells - metabolism</subject><subject>Foam Cells - pathology</subject><subject>Humans</subject><subject>Lipid accumulation</subject><subject>Lipid Metabolism - drug effects</subject><subject>Lipoproteins, LDL - metabolism</subject><subject>Lipoproteins, LDL - pharmacology</subject><subject>Liver X Receptors - metabolism</subject><subject>LXRα/ABCA1 signaling pathway</subject><subject>Muscle, Smooth, Vascular - cytology</subject><subject>Muscle, Smooth, Vascular - drug effects</subject><subject>Muscle, Smooth, Vascular - metabolism</subject><subject>Myocytes, Smooth Muscle - cytology</subject><subject>Myocytes, Smooth Muscle - drug effects</subject><subject>Myocytes, Smooth Muscle - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>Triterpenes - pharmacology</subject><subject>Vascular smooth muscle cells</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kL2O1DAURi0EYoeFF6BALmmSvXa8TizRDCP-pJGQ0BbbWY5zM_EoiYNvsmjEU_EiPBMZzUJJ5eZ8R9eHsdcCcgFC3xzzuk4-lyAhhyqHUj9hGwEGMilAPWUbANCZNOL-ir0gOgIIobR5zq4KWRlplNmwnzvsHc0p9pyWaUpIhMT7MIWGO--XYendHOLI5y7F5dDx_f23379utu93W8EpHEbXh_HAJzd3P9yJu3GdLXOcOnc48TDyB0d-VSROQ4xzx4eFfI_cY9_TS_asdT3hq8f3mt19_HC3-5ztv376stvuM1_c6jkTvqhLrYWvpDJGlFCWhQLZqhbRy8KLRhsha49StjVIVbdStd67W1VhAaa4Zm8v2inF7wvSbIdA5wPciHEhK5UCrbUq1YrKC-pTJErY2imFwaWTFWDPze3Rnpvbc3MLlV2br6M3j_6lHrD5N_kbeQXeXQBcP_kQMFnyAUePTUjoZ9vE8D__H61qlSo</recordid><startdate>20201112</startdate><enddate>20201112</enddate><creator>Shi, Yaning</creator><creator>Jiang, Shuang</creator><creator>Zhao, Tanjun</creator><creator>Gong, Yongzhen</creator><creator>Liao, Duanfang</creator><creator>Qin, Li</creator><general>Elsevier 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>7X8</scope><orcidid>https://orcid.org/0000-0002-9797-2636</orcidid></search><sort><creationdate>20201112</creationdate><title>Celastrol suppresses lipid accumulation through LXRα/ABCA1 signaling pathway and autophagy in vascular smooth muscle cells</title><author>Shi, Yaning ; Jiang, Shuang ; Zhao, Tanjun ; Gong, Yongzhen ; Liao, Duanfang ; Qin, Li</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c356t-1c3b7661c82499170773402f4feec23c1d6912bce22fb024bf24fcca548e3093</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Atherosclerosis</topic><topic>Atherosclerosis - drug therapy</topic><topic>Atherosclerosis - metabolism</topic><topic>Atherosclerosis - prevention & control</topic><topic>ATP Binding Cassette Transporter 1 - metabolism</topic><topic>Autophagy</topic><topic>Autophagy - drug effects</topic><topic>Celastrol</topic><topic>Cells, Cultured</topic><topic>Foam Cells - drug effects</topic><topic>Foam Cells - metabolism</topic><topic>Foam Cells - pathology</topic><topic>Humans</topic><topic>Lipid accumulation</topic><topic>Lipid Metabolism - drug effects</topic><topic>Lipoproteins, LDL - metabolism</topic><topic>Lipoproteins, LDL - pharmacology</topic><topic>Liver X Receptors - metabolism</topic><topic>LXRα/ABCA1 signaling pathway</topic><topic>Muscle, Smooth, Vascular - cytology</topic><topic>Muscle, Smooth, Vascular - drug effects</topic><topic>Muscle, Smooth, Vascular - metabolism</topic><topic>Myocytes, Smooth Muscle - cytology</topic><topic>Myocytes, Smooth Muscle - drug effects</topic><topic>Myocytes, Smooth Muscle - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>Triterpenes - pharmacology</topic><topic>Vascular smooth muscle cells</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shi, Yaning</creatorcontrib><creatorcontrib>Jiang, Shuang</creatorcontrib><creatorcontrib>Zhao, Tanjun</creatorcontrib><creatorcontrib>Gong, Yongzhen</creatorcontrib><creatorcontrib>Liao, Duanfang</creatorcontrib><creatorcontrib>Qin, Li</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shi, Yaning</au><au>Jiang, Shuang</au><au>Zhao, Tanjun</au><au>Gong, Yongzhen</au><au>Liao, Duanfang</au><au>Qin, Li</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Celastrol suppresses lipid accumulation through LXRα/ABCA1 signaling pathway and autophagy in vascular smooth muscle cells</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>2020-11-12</date><risdate>2020</risdate><volume>532</volume><issue>3</issue><spage>466</spage><epage>474</epage><pages>466-474</pages><issn>0006-291X</issn><eissn>1090-2104</eissn><abstract>The uptake of modified low-density lipoprotein (LDL) and the accumulation of lipid droplets induce the formation of vascular smooth muscle cells (VSMCs)-derived foam cells, thereby promoting the development and maturation of plaques and accelerating the progression of atherosclerosis. Celastrol is a quinine methide triterpenoid isolated from the root bark of traditional Chinese herb Tripterygium wilfordii. It possesses various biological properties, including anti-obesity, cardiovascular protection, anti-inflammation, etc. In the present study, we found that celastrol significantly reduced lipid accumulation induced by oxidized LDL (ox-LDL) in VSMCs. Mechanistically, celastrol up-regulated adenosine triphosphate-binding cassette transporter A1 (ABCA1) expression through activating liver X receptor α (LXRα) expression, which contributed to inhibit lipid accumulation in VSMCs. Meanwhile, celastrol decreased lipid accumulation by triggering autophagy in VSMCs. Therefore, these findings supported celastrol as a potentially effective agent for the prevention and therapy of atherosclerosis.
[Display omitted]
•Celastrol suppresses lipid accumulation by activating LXRα/ABCA1 signaling in VSMCs.•Celastrol inhibits lipid storage by inducing autophagy in VSMCs.•Celastrol is a potentially effective agent for treatment of atherosclerosis.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>32892949</pmid><doi>10.1016/j.bbrc.2020.08.076</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0002-9797-2636</orcidid></addata></record> |
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| subjects | Atherosclerosis Atherosclerosis - drug therapy Atherosclerosis - metabolism Atherosclerosis - prevention & control ATP Binding Cassette Transporter 1 - metabolism Autophagy Autophagy - drug effects Celastrol Cells, Cultured Foam Cells - drug effects Foam Cells - metabolism Foam Cells - pathology Humans Lipid accumulation Lipid Metabolism - drug effects Lipoproteins, LDL - metabolism Lipoproteins, LDL - pharmacology Liver X Receptors - metabolism LXRα/ABCA1 signaling pathway Muscle, Smooth, Vascular - cytology Muscle, Smooth, Vascular - drug effects Muscle, Smooth, Vascular - metabolism Myocytes, Smooth Muscle - cytology Myocytes, Smooth Muscle - drug effects Myocytes, Smooth Muscle - metabolism Signal Transduction - drug effects Triterpenes - pharmacology Vascular smooth muscle cells |
| title | Celastrol suppresses lipid accumulation through LXRα/ABCA1 signaling pathway and autophagy in vascular smooth muscle cells |
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