Peroxisome proliferator‐activated receptor δ improves the features of atherosclerotic plaque vulnerability by regulating smooth muscle cell phenotypic switching
Background and Purpose Vascular smooth muscle cells (SMCs) undergo phenotypic switching during sustained inflammation, contributing to an unfavourable atherosclerotic plaque phenotype. PPARδ plays an important role in regulating SMC functions; however, its role in atherosclerotic plaque vulnerabilit...
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| Veröffentlicht in: | British journal of pharmacology 2023-08, Vol.180 (16), p.2085-2101 |
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| container_title | British journal of pharmacology |
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| creator | Lien, Chih‐Feng Lin, Chin‐Sheng Shyue, Song‐Kun Hsieh, Po‐Shiuan Chen, Sy‐Jou Lin, Yi‐Tan Chien, Shu Tsai, Min‐Chien |
| description | Background and Purpose
Vascular smooth muscle cells (SMCs) undergo phenotypic switching during sustained inflammation, contributing to an unfavourable atherosclerotic plaque phenotype. PPARδ plays an important role in regulating SMC functions; however, its role in atherosclerotic plaque vulnerability remains unclear. Here, we explored the pathological roles of PPARδ in atherosclerotic plaque vulnerability in severe atherosclerosis and elucidated the underlying mechanisms.
Experimental Approach
Plasma levels of PPARδ were measured in patients with acute coronary syndrome (ACS) and stable angina (SA). SMC contractile and synthetic phenotypic markers, endoplasmic reticulum (ER) stress, and features of atherosclerotic plaque vulnerability were analysed for the brachiocephalic artery of apolipoprotein E‐knockout (ApoE−/−) mice, fed a high‐cholesterol diet (HCD) and treated with or without the PPARδ agonist GW501516. In vitro, the role of PPARδ was elucidated using human aortic SMCs (HASMCs).
Key Results
Patients with ACS had significantly lower plasma PPARδ levels than those with SA. GW501516 reduced atherosclerotic plaque vulnerability, a synthetic SMC phenotype, ER stress markers, and NLRP3 inflammasome expression in HCD‐fed ApoE−/− mice. ER stress suppressed PPARδ expression in HASMCs. PPARδ activation inhibited ER stress‐induced synthetic phenotype development, ER stress‐NLRP3 inflammasome axis activation and matrix metalloproteinase 2 (MMP2) expression in HASMCs. PPARδ inhibited NFκB signalling and alleviated ER stress‐induced SMC phenotypic switching.
Conclusions and Implications
Low plasma PPARδ levels may be associated with atherosclerotic plaque vulnerability. Our findings provide new insights into the mechanisms underlying the protective effect of PPARδ on SMC phenotypic switching and improvement the features of atherosclerotic plaque vulnerability. |
| doi_str_mv | 10.1111/bph.16074 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2789235203</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2835728553</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3884-4a74c63fb113a5256e08a27195470d1178d112381630caa1e048087e13664ab33</originalsourceid><addsrcrecordid>eNp1kUFu1TAQhi0Eoo_CggsgS2xgkdaOndhvSSugSJXoAtaR4zdpXDlxsJ1XsuMI3IErcA4OwUmY8AoLJLwYy-PPv37PT8hTzk44rtN26k94zZS8RzZcqrqohOb3yYYxpgrOtT4ij1K6YQwvVfWQHIl6K0tZiQ35dgUxfHYpDECnGLzrIJoc4s8vX43Nbm8y7GgECxM26Y_v1A2I7SHR3APtwOQ54iF01GAjhmQ91uwsnbz5NAPdz35EydZ5lxfaLih2PXuT3XhN0xBC7ukwr6-oBe_p1MMY8jKhQLp12fbIPSYPOuMTPLnbj8nHN68_nF8Ul-_fvjt_dVlYobUspFHS1qJrORemKqsamDal4ttKKrbjXGksJU6mFswaw4FJzbQCLupamlaIY_LioIs_ROspN4NLqyszQphTUyq9LUVVshV9_g96E-Y4orum1KJSpa6qlXp5oCwOJkXomim6wcSl4axZk2swueZ3csg-u1Oc2wF2f8k_USFwegBunYfl_0rN2dXFQfIX6JqnXA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2835728553</pqid></control><display><type>article</type><title>Peroxisome proliferator‐activated receptor δ improves the features of atherosclerotic plaque vulnerability by regulating smooth muscle cell phenotypic switching</title><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><source>Wiley Free Content</source><source>EZB-FREE-00999 freely available EZB journals</source><source>Alma/SFX Local Collection</source><creator>Lien, Chih‐Feng ; Lin, Chin‐Sheng ; Shyue, Song‐Kun ; Hsieh, Po‐Shiuan ; Chen, Sy‐Jou ; Lin, Yi‐Tan ; Chien, Shu ; Tsai, Min‐Chien</creator><creatorcontrib>Lien, Chih‐Feng ; Lin, Chin‐Sheng ; Shyue, Song‐Kun ; Hsieh, Po‐Shiuan ; Chen, Sy‐Jou ; Lin, Yi‐Tan ; Chien, Shu ; Tsai, Min‐Chien</creatorcontrib><description>Background and Purpose
Vascular smooth muscle cells (SMCs) undergo phenotypic switching during sustained inflammation, contributing to an unfavourable atherosclerotic plaque phenotype. PPARδ plays an important role in regulating SMC functions; however, its role in atherosclerotic plaque vulnerability remains unclear. Here, we explored the pathological roles of PPARδ in atherosclerotic plaque vulnerability in severe atherosclerosis and elucidated the underlying mechanisms.
Experimental Approach
Plasma levels of PPARδ were measured in patients with acute coronary syndrome (ACS) and stable angina (SA). SMC contractile and synthetic phenotypic markers, endoplasmic reticulum (ER) stress, and features of atherosclerotic plaque vulnerability were analysed for the brachiocephalic artery of apolipoprotein E‐knockout (ApoE−/−) mice, fed a high‐cholesterol diet (HCD) and treated with or without the PPARδ agonist GW501516. In vitro, the role of PPARδ was elucidated using human aortic SMCs (HASMCs).
Key Results
Patients with ACS had significantly lower plasma PPARδ levels than those with SA. GW501516 reduced atherosclerotic plaque vulnerability, a synthetic SMC phenotype, ER stress markers, and NLRP3 inflammasome expression in HCD‐fed ApoE−/− mice. ER stress suppressed PPARδ expression in HASMCs. PPARδ activation inhibited ER stress‐induced synthetic phenotype development, ER stress‐NLRP3 inflammasome axis activation and matrix metalloproteinase 2 (MMP2) expression in HASMCs. PPARδ inhibited NFκB signalling and alleviated ER stress‐induced SMC phenotypic switching.
Conclusions and Implications
Low plasma PPARδ levels may be associated with atherosclerotic plaque vulnerability. Our findings provide new insights into the mechanisms underlying the protective effect of PPARδ on SMC phenotypic switching and improvement the features of atherosclerotic plaque vulnerability.</description><identifier>ISSN: 0007-1188</identifier><identifier>EISSN: 1476-5381</identifier><identifier>DOI: 10.1111/bph.16074</identifier><identifier>PMID: 36942453</identifier><language>eng</language><publisher>England: Blackwell Publishing Ltd</publisher><subject>acute coronary syndrome ; Acute coronary syndromes ; Angina ; Animals ; Aorta ; Apolipoprotein E ; Apolipoproteins E - genetics ; Apolipoproteins E - metabolism ; Arteriosclerosis ; Atherosclerosis ; atherosclerotic plaque vulnerability ; Cholesterol ; Endoplasmic reticulum ; endoplasmic reticulum stress ; Gelatinase A ; Genotype & phenotype ; High cholesterol diet ; Humans ; Inflammasomes ; Inflammasomes - metabolism ; Matrix metalloproteinase ; Matrix Metalloproteinase 2 - metabolism ; Metalloproteinase ; Mice ; Mice, Inbred C57BL ; Muscle contraction ; Myocytes, Smooth Muscle - metabolism ; NF-κB protein ; NLR Family, Pyrin Domain-Containing 3 Protein - metabolism ; Peroxisome proliferator-activated receptors ; Phenotype ; Phenotypes ; phenotypic switching ; Plaque, Atherosclerotic - metabolism ; Plasma levels ; PPAR delta - genetics ; PPARδ ; Smooth muscle ; smooth muscle cell</subject><ispartof>British journal of pharmacology, 2023-08, Vol.180 (16), p.2085-2101</ispartof><rights>2023 British Pharmacological Society.</rights><rights>2023 The British Pharmacological Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3884-4a74c63fb113a5256e08a27195470d1178d112381630caa1e048087e13664ab33</citedby><cites>FETCH-LOGICAL-c3884-4a74c63fb113a5256e08a27195470d1178d112381630caa1e048087e13664ab33</cites><orcidid>0000-0002-5167-8327 ; 0000-0002-2869-2382</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fbph.16074$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fbph.16074$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,1427,27903,27904,45553,45554,46388,46812</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36942453$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lien, Chih‐Feng</creatorcontrib><creatorcontrib>Lin, Chin‐Sheng</creatorcontrib><creatorcontrib>Shyue, Song‐Kun</creatorcontrib><creatorcontrib>Hsieh, Po‐Shiuan</creatorcontrib><creatorcontrib>Chen, Sy‐Jou</creatorcontrib><creatorcontrib>Lin, Yi‐Tan</creatorcontrib><creatorcontrib>Chien, Shu</creatorcontrib><creatorcontrib>Tsai, Min‐Chien</creatorcontrib><title>Peroxisome proliferator‐activated receptor δ improves the features of atherosclerotic plaque vulnerability by regulating smooth muscle cell phenotypic switching</title><title>British journal of pharmacology</title><addtitle>Br J Pharmacol</addtitle><description>Background and Purpose
Vascular smooth muscle cells (SMCs) undergo phenotypic switching during sustained inflammation, contributing to an unfavourable atherosclerotic plaque phenotype. PPARδ plays an important role in regulating SMC functions; however, its role in atherosclerotic plaque vulnerability remains unclear. Here, we explored the pathological roles of PPARδ in atherosclerotic plaque vulnerability in severe atherosclerosis and elucidated the underlying mechanisms.
Experimental Approach
Plasma levels of PPARδ were measured in patients with acute coronary syndrome (ACS) and stable angina (SA). SMC contractile and synthetic phenotypic markers, endoplasmic reticulum (ER) stress, and features of atherosclerotic plaque vulnerability were analysed for the brachiocephalic artery of apolipoprotein E‐knockout (ApoE−/−) mice, fed a high‐cholesterol diet (HCD) and treated with or without the PPARδ agonist GW501516. In vitro, the role of PPARδ was elucidated using human aortic SMCs (HASMCs).
Key Results
Patients with ACS had significantly lower plasma PPARδ levels than those with SA. GW501516 reduced atherosclerotic plaque vulnerability, a synthetic SMC phenotype, ER stress markers, and NLRP3 inflammasome expression in HCD‐fed ApoE−/− mice. ER stress suppressed PPARδ expression in HASMCs. PPARδ activation inhibited ER stress‐induced synthetic phenotype development, ER stress‐NLRP3 inflammasome axis activation and matrix metalloproteinase 2 (MMP2) expression in HASMCs. PPARδ inhibited NFκB signalling and alleviated ER stress‐induced SMC phenotypic switching.
Conclusions and Implications
Low plasma PPARδ levels may be associated with atherosclerotic plaque vulnerability. Our findings provide new insights into the mechanisms underlying the protective effect of PPARδ on SMC phenotypic switching and improvement the features of atherosclerotic plaque vulnerability.</description><subject>acute coronary syndrome</subject><subject>Acute coronary syndromes</subject><subject>Angina</subject><subject>Animals</subject><subject>Aorta</subject><subject>Apolipoprotein E</subject><subject>Apolipoproteins E - genetics</subject><subject>Apolipoproteins E - metabolism</subject><subject>Arteriosclerosis</subject><subject>Atherosclerosis</subject><subject>atherosclerotic plaque vulnerability</subject><subject>Cholesterol</subject><subject>Endoplasmic reticulum</subject><subject>endoplasmic reticulum stress</subject><subject>Gelatinase A</subject><subject>Genotype & phenotype</subject><subject>High cholesterol diet</subject><subject>Humans</subject><subject>Inflammasomes</subject><subject>Inflammasomes - metabolism</subject><subject>Matrix metalloproteinase</subject><subject>Matrix Metalloproteinase 2 - metabolism</subject><subject>Metalloproteinase</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Muscle contraction</subject><subject>Myocytes, Smooth Muscle - metabolism</subject><subject>NF-κB protein</subject><subject>NLR Family, Pyrin Domain-Containing 3 Protein - metabolism</subject><subject>Peroxisome proliferator-activated receptors</subject><subject>Phenotype</subject><subject>Phenotypes</subject><subject>phenotypic switching</subject><subject>Plaque, Atherosclerotic - metabolism</subject><subject>Plasma levels</subject><subject>PPAR delta - genetics</subject><subject>PPARδ</subject><subject>Smooth muscle</subject><subject>smooth muscle cell</subject><issn>0007-1188</issn><issn>1476-5381</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kUFu1TAQhi0Eoo_CggsgS2xgkdaOndhvSSugSJXoAtaR4zdpXDlxsJ1XsuMI3IErcA4OwUmY8AoLJLwYy-PPv37PT8hTzk44rtN26k94zZS8RzZcqrqohOb3yYYxpgrOtT4ij1K6YQwvVfWQHIl6K0tZiQ35dgUxfHYpDECnGLzrIJoc4s8vX43Nbm8y7GgECxM26Y_v1A2I7SHR3APtwOQ54iF01GAjhmQ91uwsnbz5NAPdz35EydZ5lxfaLih2PXuT3XhN0xBC7ukwr6-oBe_p1MMY8jKhQLp12fbIPSYPOuMTPLnbj8nHN68_nF8Ul-_fvjt_dVlYobUspFHS1qJrORemKqsamDal4ttKKrbjXGksJU6mFswaw4FJzbQCLupamlaIY_LioIs_ROspN4NLqyszQphTUyq9LUVVshV9_g96E-Y4orum1KJSpa6qlXp5oCwOJkXomim6wcSl4axZk2swueZ3csg-u1Oc2wF2f8k_USFwegBunYfl_0rN2dXFQfIX6JqnXA</recordid><startdate>202308</startdate><enddate>202308</enddate><creator>Lien, Chih‐Feng</creator><creator>Lin, Chin‐Sheng</creator><creator>Shyue, Song‐Kun</creator><creator>Hsieh, Po‐Shiuan</creator><creator>Chen, Sy‐Jou</creator><creator>Lin, Yi‐Tan</creator><creator>Chien, Shu</creator><creator>Tsai, Min‐Chien</creator><general>Blackwell Publishing Ltd</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>7QP</scope><scope>7TK</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-5167-8327</orcidid><orcidid>https://orcid.org/0000-0002-2869-2382</orcidid></search><sort><creationdate>202308</creationdate><title>Peroxisome proliferator‐activated receptor δ improves the features of atherosclerotic plaque vulnerability by regulating smooth muscle cell phenotypic switching</title><author>Lien, Chih‐Feng ; Lin, Chin‐Sheng ; Shyue, Song‐Kun ; Hsieh, Po‐Shiuan ; Chen, Sy‐Jou ; Lin, Yi‐Tan ; Chien, Shu ; Tsai, Min‐Chien</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3884-4a74c63fb113a5256e08a27195470d1178d112381630caa1e048087e13664ab33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>acute coronary syndrome</topic><topic>Acute coronary syndromes</topic><topic>Angina</topic><topic>Animals</topic><topic>Aorta</topic><topic>Apolipoprotein E</topic><topic>Apolipoproteins E - genetics</topic><topic>Apolipoproteins E - metabolism</topic><topic>Arteriosclerosis</topic><topic>Atherosclerosis</topic><topic>atherosclerotic plaque vulnerability</topic><topic>Cholesterol</topic><topic>Endoplasmic reticulum</topic><topic>endoplasmic reticulum stress</topic><topic>Gelatinase A</topic><topic>Genotype & phenotype</topic><topic>High cholesterol diet</topic><topic>Humans</topic><topic>Inflammasomes</topic><topic>Inflammasomes - metabolism</topic><topic>Matrix metalloproteinase</topic><topic>Matrix Metalloproteinase 2 - metabolism</topic><topic>Metalloproteinase</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Muscle contraction</topic><topic>Myocytes, Smooth Muscle - metabolism</topic><topic>NF-κB protein</topic><topic>NLR Family, Pyrin Domain-Containing 3 Protein - metabolism</topic><topic>Peroxisome proliferator-activated receptors</topic><topic>Phenotype</topic><topic>Phenotypes</topic><topic>phenotypic switching</topic><topic>Plaque, Atherosclerotic - metabolism</topic><topic>Plasma levels</topic><topic>PPAR delta - genetics</topic><topic>PPARδ</topic><topic>Smooth muscle</topic><topic>smooth muscle cell</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lien, Chih‐Feng</creatorcontrib><creatorcontrib>Lin, Chin‐Sheng</creatorcontrib><creatorcontrib>Shyue, Song‐Kun</creatorcontrib><creatorcontrib>Hsieh, Po‐Shiuan</creatorcontrib><creatorcontrib>Chen, Sy‐Jou</creatorcontrib><creatorcontrib>Lin, Yi‐Tan</creatorcontrib><creatorcontrib>Chien, Shu</creatorcontrib><creatorcontrib>Tsai, Min‐Chien</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>British journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lien, Chih‐Feng</au><au>Lin, Chin‐Sheng</au><au>Shyue, Song‐Kun</au><au>Hsieh, Po‐Shiuan</au><au>Chen, Sy‐Jou</au><au>Lin, Yi‐Tan</au><au>Chien, Shu</au><au>Tsai, Min‐Chien</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Peroxisome proliferator‐activated receptor δ improves the features of atherosclerotic plaque vulnerability by regulating smooth muscle cell phenotypic switching</atitle><jtitle>British journal of pharmacology</jtitle><addtitle>Br J Pharmacol</addtitle><date>2023-08</date><risdate>2023</risdate><volume>180</volume><issue>16</issue><spage>2085</spage><epage>2101</epage><pages>2085-2101</pages><issn>0007-1188</issn><eissn>1476-5381</eissn><abstract>Background and Purpose
Vascular smooth muscle cells (SMCs) undergo phenotypic switching during sustained inflammation, contributing to an unfavourable atherosclerotic plaque phenotype. PPARδ plays an important role in regulating SMC functions; however, its role in atherosclerotic plaque vulnerability remains unclear. Here, we explored the pathological roles of PPARδ in atherosclerotic plaque vulnerability in severe atherosclerosis and elucidated the underlying mechanisms.
Experimental Approach
Plasma levels of PPARδ were measured in patients with acute coronary syndrome (ACS) and stable angina (SA). SMC contractile and synthetic phenotypic markers, endoplasmic reticulum (ER) stress, and features of atherosclerotic plaque vulnerability were analysed for the brachiocephalic artery of apolipoprotein E‐knockout (ApoE−/−) mice, fed a high‐cholesterol diet (HCD) and treated with or without the PPARδ agonist GW501516. In vitro, the role of PPARδ was elucidated using human aortic SMCs (HASMCs).
Key Results
Patients with ACS had significantly lower plasma PPARδ levels than those with SA. GW501516 reduced atherosclerotic plaque vulnerability, a synthetic SMC phenotype, ER stress markers, and NLRP3 inflammasome expression in HCD‐fed ApoE−/− mice. ER stress suppressed PPARδ expression in HASMCs. PPARδ activation inhibited ER stress‐induced synthetic phenotype development, ER stress‐NLRP3 inflammasome axis activation and matrix metalloproteinase 2 (MMP2) expression in HASMCs. PPARδ inhibited NFκB signalling and alleviated ER stress‐induced SMC phenotypic switching.
Conclusions and Implications
Low plasma PPARδ levels may be associated with atherosclerotic plaque vulnerability. Our findings provide new insights into the mechanisms underlying the protective effect of PPARδ on SMC phenotypic switching and improvement the features of atherosclerotic plaque vulnerability.</abstract><cop>England</cop><pub>Blackwell Publishing Ltd</pub><pmid>36942453</pmid><doi>10.1111/bph.16074</doi><tpages>17</tpages><orcidid>https://orcid.org/0000-0002-5167-8327</orcidid><orcidid>https://orcid.org/0000-0002-2869-2382</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | acute coronary syndrome Acute coronary syndromes Angina Animals Aorta Apolipoprotein E Apolipoproteins E - genetics Apolipoproteins E - metabolism Arteriosclerosis Atherosclerosis atherosclerotic plaque vulnerability Cholesterol Endoplasmic reticulum endoplasmic reticulum stress Gelatinase A Genotype & phenotype High cholesterol diet Humans Inflammasomes Inflammasomes - metabolism Matrix metalloproteinase Matrix Metalloproteinase 2 - metabolism Metalloproteinase Mice Mice, Inbred C57BL Muscle contraction Myocytes, Smooth Muscle - metabolism NF-κB protein NLR Family, Pyrin Domain-Containing 3 Protein - metabolism Peroxisome proliferator-activated receptors Phenotype Phenotypes phenotypic switching Plaque, Atherosclerotic - metabolism Plasma levels PPAR delta - genetics PPARδ Smooth muscle smooth muscle cell |
| title | Peroxisome proliferator‐activated receptor δ improves the features of atherosclerotic plaque vulnerability by regulating smooth muscle cell phenotypic switching |
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