Adrenomedullin, transcriptionally regulated by vitamin D receptors, alleviates atherosclerosis in mice through suppressing AMPK‐mediated endothelial ferroptosis
Purpose Vitamin D receptors (VDR) play important roles in cardiovascular, immune, metabolic and other functions. Activation of VDR may help improve endothelial dysfunction, atherosclerosis, vascular calcification, and cardiac hypertrophy. However, the specific target genes and mechanisms of VDR in i...
Gespeichert in:
| Veröffentlicht in: | Environmental toxicology 2024-01, Vol.39 (1), p.199-211 |
|---|---|
| Hauptverfasser: | , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 211 |
|---|---|
| container_issue | 1 |
| container_start_page | 199 |
| container_title | Environmental toxicology |
| container_volume | 39 |
| creator | Hu, Yanchao Gu, Xu Zhang, Yan Ma, Weidong Sun, Lijun Wang, Congxia Ren, Bincheng |
| description | Purpose
Vitamin D receptors (VDR) play important roles in cardiovascular, immune, metabolic and other functions. Activation of VDR may help improve endothelial dysfunction, atherosclerosis, vascular calcification, and cardiac hypertrophy. However, the specific target genes and mechanisms of VDR in improving Human Umbilical Vein Endothelial Cell (HUVEC) functions remain unclear. This study aims to investigate the function and mechanism of VDR in HUVECs.
Methods
Endothelial dysfunction cell model was constructed by oxidized low‐density lipoprotein (ox‐LDL). An animal model of atherosclerosis was established in male homozygous Apoe−/− mice (6 weeks) on a high fat diet for 6 weeks. The relationship between VDR and adrenomedullin (ADM) was studied by bioinformatics analysis, ChIP, and luciferase reporter gene analysis. Endothelial cell function was evaluated by Transwell migration and Tube Formation tests. Ferroptosis was detected by measuring intracellular iron content, levels of oxidative stress markers, and ferroptosis related proteins.
Results
Overexpression of VDR in HUVECs inhibits ox‐LDL‐induced endothelial dysfunction and ferroptosis. VDR binds to the ADM promoter sequence and regulates the transcription of ADM. Inhibition of ADM promotes ox‐LDL‐induced endothelial dysfunction and ferroptosis. ADM regulates ox‐LDL‐induced endothelial dysfunction and ferroptosis through the AMPK signaling pathway. Overexpression of VDR in Apoe−/− mice inhibited lipid deposition and plaque area in atherosclerotic mice.
Conclusion
VDR inhibits ox‐LDL‐induced endothelial dysfunction and ferroptosis by regulating ADM transcription and acting on AMPK signaling pathway. Overexpression of VDR in Apoe−/− mice reduced lipid deposition and plaque area in the thoracic aorta of atherosclerotic mice. |
| doi_str_mv | 10.1002/tox.23958 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2863297157</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2863297157</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3888-72052bf4ffcaf083e98b95fb1efc94abaa72cc84e35b79d5e7644075d75e049d3</originalsourceid><addsrcrecordid>eNp1kc9OHCEcx4lpo1Z78AUakl40cZVhhgGOG7V_Uht7sElvE4b5sYthhhEY2731EfoMfbQ-Sdld66GJFyDkw-cXvl-EjgpyVhBCz5P_cUZLycQO2i8YpTNOuXixOZNZRUSxh17FeEcIkTWrd9FeyWshuCj30e95F2DwPXSTc3Y4xSmoIepgx2T9oJxb4QCLyakEHW5X-MEm1dsBX-ZrDWPyIZ7ijMGDzUjEKi0h-KjderURZ7S3GnBaBj8tljhO4xggRjss8Pzzl09_fv7Ks-1GD0Pn83NnlcMGQvBZnx2H6KVRLsLrx_0AfX13dXvxYXZ98_7jxfx6pkshRP4zYbQ1lTFaGSJKkKKVzLQFGC0r1SrFqdaigpK1XHYMeF1VhLOOMyCV7MoDdLz1jsHfTxBT09uowTk1gJ9iQ0VdUskLxjP69j_0zk8hx5UpSRgjUhZr6mRL6ZxFDGCaMdhehVVTkGZdXJOLazbFZfbNo3FqcyBP5L-mMnC-Bb5bB6vnTc3tzbet8i8F86iH</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2905509917</pqid></control><display><type>article</type><title>Adrenomedullin, transcriptionally regulated by vitamin D receptors, alleviates atherosclerosis in mice through suppressing AMPK‐mediated endothelial ferroptosis</title><source>Wiley Online Library - AutoHoldings Journals</source><source>MEDLINE</source><creator>Hu, Yanchao ; Gu, Xu ; Zhang, Yan ; Ma, Weidong ; Sun, Lijun ; Wang, Congxia ; Ren, Bincheng</creator><creatorcontrib>Hu, Yanchao ; Gu, Xu ; Zhang, Yan ; Ma, Weidong ; Sun, Lijun ; Wang, Congxia ; Ren, Bincheng</creatorcontrib><description>Purpose
Vitamin D receptors (VDR) play important roles in cardiovascular, immune, metabolic and other functions. Activation of VDR may help improve endothelial dysfunction, atherosclerosis, vascular calcification, and cardiac hypertrophy. However, the specific target genes and mechanisms of VDR in improving Human Umbilical Vein Endothelial Cell (HUVEC) functions remain unclear. This study aims to investigate the function and mechanism of VDR in HUVECs.
Methods
Endothelial dysfunction cell model was constructed by oxidized low‐density lipoprotein (ox‐LDL). An animal model of atherosclerosis was established in male homozygous Apoe−/− mice (6 weeks) on a high fat diet for 6 weeks. The relationship between VDR and adrenomedullin (ADM) was studied by bioinformatics analysis, ChIP, and luciferase reporter gene analysis. Endothelial cell function was evaluated by Transwell migration and Tube Formation tests. Ferroptosis was detected by measuring intracellular iron content, levels of oxidative stress markers, and ferroptosis related proteins.
Results
Overexpression of VDR in HUVECs inhibits ox‐LDL‐induced endothelial dysfunction and ferroptosis. VDR binds to the ADM promoter sequence and regulates the transcription of ADM. Inhibition of ADM promotes ox‐LDL‐induced endothelial dysfunction and ferroptosis. ADM regulates ox‐LDL‐induced endothelial dysfunction and ferroptosis through the AMPK signaling pathway. Overexpression of VDR in Apoe−/− mice inhibited lipid deposition and plaque area in atherosclerotic mice.
Conclusion
VDR inhibits ox‐LDL‐induced endothelial dysfunction and ferroptosis by regulating ADM transcription and acting on AMPK signaling pathway. Overexpression of VDR in Apoe−/− mice reduced lipid deposition and plaque area in the thoracic aorta of atherosclerotic mice.</description><identifier>ISSN: 1520-4081</identifier><identifier>EISSN: 1522-7278</identifier><identifier>DOI: 10.1002/tox.23958</identifier><identifier>PMID: 37688783</identifier><language>eng</language><publisher>Hoboken, USA: John Wiley & Sons, Inc</publisher><subject>ADM ; Adrenomedullin ; Adrenomedullin - genetics ; Adrenomedullin - metabolism ; AMP-Activated Protein Kinases - genetics ; AMP-Activated Protein Kinases - metabolism ; Animal models ; Animals ; Aorta ; Apolipoprotein E ; Apolipoproteins E - genetics ; Apolipoproteins E - metabolism ; Apoptosis ; Arteriosclerosis ; Atherosclerosis ; Atherosclerosis - genetics ; Atherosclerosis - metabolism ; Bioinformatics ; Calciferol ; Calcification ; Calcification (ectopic) ; Deposition ; Endothelial cells ; endothelial dysfunction ; Ferroptosis ; High fat diet ; Human Umbilical Vein Endothelial Cells - metabolism ; Humans ; Hypertrophy ; Lipids ; Lipoproteins ; Male ; Metabolic rate ; Mice ; Mice, Knockout, ApoE ; MicroRNAs - metabolism ; Oxidative stress ; Receptors ; Receptors, Calcitriol - genetics ; Receptors, Calcitriol - metabolism ; Reporter gene ; Signal transduction ; Thorax ; Transcription ; Umbilical cables ; Umbilical vein ; VDR ; Vitamin D ; Vitamin D receptors ; Vitamins</subject><ispartof>Environmental toxicology, 2024-01, Vol.39 (1), p.199-211</ispartof><rights>2023 Wiley Periodicals LLC.</rights><rights>2024 Wiley Periodicals LLC.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3888-72052bf4ffcaf083e98b95fb1efc94abaa72cc84e35b79d5e7644075d75e049d3</citedby><cites>FETCH-LOGICAL-c3888-72052bf4ffcaf083e98b95fb1efc94abaa72cc84e35b79d5e7644075d75e049d3</cites><orcidid>0000-0001-9985-9867</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%2Ftox.23958$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Ftox.23958$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>315,781,785,1418,27929,27930,45579,45580</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37688783$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hu, Yanchao</creatorcontrib><creatorcontrib>Gu, Xu</creatorcontrib><creatorcontrib>Zhang, Yan</creatorcontrib><creatorcontrib>Ma, Weidong</creatorcontrib><creatorcontrib>Sun, Lijun</creatorcontrib><creatorcontrib>Wang, Congxia</creatorcontrib><creatorcontrib>Ren, Bincheng</creatorcontrib><title>Adrenomedullin, transcriptionally regulated by vitamin D receptors, alleviates atherosclerosis in mice through suppressing AMPK‐mediated endothelial ferroptosis</title><title>Environmental toxicology</title><addtitle>Environ Toxicol</addtitle><description>Purpose
Vitamin D receptors (VDR) play important roles in cardiovascular, immune, metabolic and other functions. Activation of VDR may help improve endothelial dysfunction, atherosclerosis, vascular calcification, and cardiac hypertrophy. However, the specific target genes and mechanisms of VDR in improving Human Umbilical Vein Endothelial Cell (HUVEC) functions remain unclear. This study aims to investigate the function and mechanism of VDR in HUVECs.
Methods
Endothelial dysfunction cell model was constructed by oxidized low‐density lipoprotein (ox‐LDL). An animal model of atherosclerosis was established in male homozygous Apoe−/− mice (6 weeks) on a high fat diet for 6 weeks. The relationship between VDR and adrenomedullin (ADM) was studied by bioinformatics analysis, ChIP, and luciferase reporter gene analysis. Endothelial cell function was evaluated by Transwell migration and Tube Formation tests. Ferroptosis was detected by measuring intracellular iron content, levels of oxidative stress markers, and ferroptosis related proteins.
Results
Overexpression of VDR in HUVECs inhibits ox‐LDL‐induced endothelial dysfunction and ferroptosis. VDR binds to the ADM promoter sequence and regulates the transcription of ADM. Inhibition of ADM promotes ox‐LDL‐induced endothelial dysfunction and ferroptosis. ADM regulates ox‐LDL‐induced endothelial dysfunction and ferroptosis through the AMPK signaling pathway. Overexpression of VDR in Apoe−/− mice inhibited lipid deposition and plaque area in atherosclerotic mice.
Conclusion
VDR inhibits ox‐LDL‐induced endothelial dysfunction and ferroptosis by regulating ADM transcription and acting on AMPK signaling pathway. Overexpression of VDR in Apoe−/− mice reduced lipid deposition and plaque area in the thoracic aorta of atherosclerotic mice.</description><subject>ADM</subject><subject>Adrenomedullin</subject><subject>Adrenomedullin - genetics</subject><subject>Adrenomedullin - metabolism</subject><subject>AMP-Activated Protein Kinases - genetics</subject><subject>AMP-Activated Protein Kinases - metabolism</subject><subject>Animal models</subject><subject>Animals</subject><subject>Aorta</subject><subject>Apolipoprotein E</subject><subject>Apolipoproteins E - genetics</subject><subject>Apolipoproteins E - metabolism</subject><subject>Apoptosis</subject><subject>Arteriosclerosis</subject><subject>Atherosclerosis</subject><subject>Atherosclerosis - genetics</subject><subject>Atherosclerosis - metabolism</subject><subject>Bioinformatics</subject><subject>Calciferol</subject><subject>Calcification</subject><subject>Calcification (ectopic)</subject><subject>Deposition</subject><subject>Endothelial cells</subject><subject>endothelial dysfunction</subject><subject>Ferroptosis</subject><subject>High fat diet</subject><subject>Human Umbilical Vein Endothelial Cells - metabolism</subject><subject>Humans</subject><subject>Hypertrophy</subject><subject>Lipids</subject><subject>Lipoproteins</subject><subject>Male</subject><subject>Metabolic rate</subject><subject>Mice</subject><subject>Mice, Knockout, ApoE</subject><subject>MicroRNAs - metabolism</subject><subject>Oxidative stress</subject><subject>Receptors</subject><subject>Receptors, Calcitriol - genetics</subject><subject>Receptors, Calcitriol - metabolism</subject><subject>Reporter gene</subject><subject>Signal transduction</subject><subject>Thorax</subject><subject>Transcription</subject><subject>Umbilical cables</subject><subject>Umbilical vein</subject><subject>VDR</subject><subject>Vitamin D</subject><subject>Vitamin D receptors</subject><subject>Vitamins</subject><issn>1520-4081</issn><issn>1522-7278</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kc9OHCEcx4lpo1Z78AUakl40cZVhhgGOG7V_Uht7sElvE4b5sYthhhEY2731EfoMfbQ-Sdld66GJFyDkw-cXvl-EjgpyVhBCz5P_cUZLycQO2i8YpTNOuXixOZNZRUSxh17FeEcIkTWrd9FeyWshuCj30e95F2DwPXSTc3Y4xSmoIepgx2T9oJxb4QCLyakEHW5X-MEm1dsBX-ZrDWPyIZ7ijMGDzUjEKi0h-KjderURZ7S3GnBaBj8tljhO4xggRjss8Pzzl09_fv7Ks-1GD0Pn83NnlcMGQvBZnx2H6KVRLsLrx_0AfX13dXvxYXZ98_7jxfx6pkshRP4zYbQ1lTFaGSJKkKKVzLQFGC0r1SrFqdaigpK1XHYMeF1VhLOOMyCV7MoDdLz1jsHfTxBT09uowTk1gJ9iQ0VdUskLxjP69j_0zk8hx5UpSRgjUhZr6mRL6ZxFDGCaMdhehVVTkGZdXJOLazbFZfbNo3FqcyBP5L-mMnC-Bb5bB6vnTc3tzbet8i8F86iH</recordid><startdate>202401</startdate><enddate>202401</enddate><creator>Hu, Yanchao</creator><creator>Gu, Xu</creator><creator>Zhang, Yan</creator><creator>Ma, Weidong</creator><creator>Sun, Lijun</creator><creator>Wang, Congxia</creator><creator>Ren, Bincheng</creator><general>John Wiley & Sons, Inc</general><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>7QH</scope><scope>7ST</scope><scope>7TN</scope><scope>7U7</scope><scope>7UA</scope><scope>C1K</scope><scope>F1W</scope><scope>H97</scope><scope>K9.</scope><scope>L.G</scope><scope>M7N</scope><scope>SOI</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-9985-9867</orcidid></search><sort><creationdate>202401</creationdate><title>Adrenomedullin, transcriptionally regulated by vitamin D receptors, alleviates atherosclerosis in mice through suppressing AMPK‐mediated endothelial ferroptosis</title><author>Hu, Yanchao ; Gu, Xu ; Zhang, Yan ; Ma, Weidong ; Sun, Lijun ; Wang, Congxia ; Ren, Bincheng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3888-72052bf4ffcaf083e98b95fb1efc94abaa72cc84e35b79d5e7644075d75e049d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>ADM</topic><topic>Adrenomedullin</topic><topic>Adrenomedullin - genetics</topic><topic>Adrenomedullin - metabolism</topic><topic>AMP-Activated Protein Kinases - genetics</topic><topic>AMP-Activated Protein Kinases - metabolism</topic><topic>Animal models</topic><topic>Animals</topic><topic>Aorta</topic><topic>Apolipoprotein E</topic><topic>Apolipoproteins E - genetics</topic><topic>Apolipoproteins E - metabolism</topic><topic>Apoptosis</topic><topic>Arteriosclerosis</topic><topic>Atherosclerosis</topic><topic>Atherosclerosis - genetics</topic><topic>Atherosclerosis - metabolism</topic><topic>Bioinformatics</topic><topic>Calciferol</topic><topic>Calcification</topic><topic>Calcification (ectopic)</topic><topic>Deposition</topic><topic>Endothelial cells</topic><topic>endothelial dysfunction</topic><topic>Ferroptosis</topic><topic>High fat diet</topic><topic>Human Umbilical Vein Endothelial Cells - metabolism</topic><topic>Humans</topic><topic>Hypertrophy</topic><topic>Lipids</topic><topic>Lipoproteins</topic><topic>Male</topic><topic>Metabolic rate</topic><topic>Mice</topic><topic>Mice, Knockout, ApoE</topic><topic>MicroRNAs - metabolism</topic><topic>Oxidative stress</topic><topic>Receptors</topic><topic>Receptors, Calcitriol - genetics</topic><topic>Receptors, Calcitriol - metabolism</topic><topic>Reporter gene</topic><topic>Signal transduction</topic><topic>Thorax</topic><topic>Transcription</topic><topic>Umbilical cables</topic><topic>Umbilical vein</topic><topic>VDR</topic><topic>Vitamin D</topic><topic>Vitamin D receptors</topic><topic>Vitamins</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hu, Yanchao</creatorcontrib><creatorcontrib>Gu, Xu</creatorcontrib><creatorcontrib>Zhang, Yan</creatorcontrib><creatorcontrib>Ma, Weidong</creatorcontrib><creatorcontrib>Sun, Lijun</creatorcontrib><creatorcontrib>Wang, Congxia</creatorcontrib><creatorcontrib>Ren, Bincheng</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Aqualine</collection><collection>Environment Abstracts</collection><collection>Oceanic Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Water Resources Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ASFA: Aquatic Sciences and Fisheries Abstracts</collection><collection>Aquatic Science & Fisheries Abstracts (ASFA) 3: Aquatic Pollution & Environmental Quality</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Aquatic Science & Fisheries Abstracts (ASFA) Professional</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Environment Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Environmental toxicology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hu, Yanchao</au><au>Gu, Xu</au><au>Zhang, Yan</au><au>Ma, Weidong</au><au>Sun, Lijun</au><au>Wang, Congxia</au><au>Ren, Bincheng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Adrenomedullin, transcriptionally regulated by vitamin D receptors, alleviates atherosclerosis in mice through suppressing AMPK‐mediated endothelial ferroptosis</atitle><jtitle>Environmental toxicology</jtitle><addtitle>Environ Toxicol</addtitle><date>2024-01</date><risdate>2024</risdate><volume>39</volume><issue>1</issue><spage>199</spage><epage>211</epage><pages>199-211</pages><issn>1520-4081</issn><eissn>1522-7278</eissn><abstract>Purpose
Vitamin D receptors (VDR) play important roles in cardiovascular, immune, metabolic and other functions. Activation of VDR may help improve endothelial dysfunction, atherosclerosis, vascular calcification, and cardiac hypertrophy. However, the specific target genes and mechanisms of VDR in improving Human Umbilical Vein Endothelial Cell (HUVEC) functions remain unclear. This study aims to investigate the function and mechanism of VDR in HUVECs.
Methods
Endothelial dysfunction cell model was constructed by oxidized low‐density lipoprotein (ox‐LDL). An animal model of atherosclerosis was established in male homozygous Apoe−/− mice (6 weeks) on a high fat diet for 6 weeks. The relationship between VDR and adrenomedullin (ADM) was studied by bioinformatics analysis, ChIP, and luciferase reporter gene analysis. Endothelial cell function was evaluated by Transwell migration and Tube Formation tests. Ferroptosis was detected by measuring intracellular iron content, levels of oxidative stress markers, and ferroptosis related proteins.
Results
Overexpression of VDR in HUVECs inhibits ox‐LDL‐induced endothelial dysfunction and ferroptosis. VDR binds to the ADM promoter sequence and regulates the transcription of ADM. Inhibition of ADM promotes ox‐LDL‐induced endothelial dysfunction and ferroptosis. ADM regulates ox‐LDL‐induced endothelial dysfunction and ferroptosis through the AMPK signaling pathway. Overexpression of VDR in Apoe−/− mice inhibited lipid deposition and plaque area in atherosclerotic mice.
Conclusion
VDR inhibits ox‐LDL‐induced endothelial dysfunction and ferroptosis by regulating ADM transcription and acting on AMPK signaling pathway. Overexpression of VDR in Apoe−/− mice reduced lipid deposition and plaque area in the thoracic aorta of atherosclerotic mice.</abstract><cop>Hoboken, USA</cop><pub>John Wiley & Sons, Inc</pub><pmid>37688783</pmid><doi>10.1002/tox.23958</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0001-9985-9867</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1520-4081 |
| ispartof | Environmental toxicology, 2024-01, Vol.39 (1), p.199-211 |
| issn | 1520-4081 1522-7278 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_2863297157 |
| source | Wiley Online Library - AutoHoldings Journals; MEDLINE |
| subjects | ADM Adrenomedullin Adrenomedullin - genetics Adrenomedullin - metabolism AMP-Activated Protein Kinases - genetics AMP-Activated Protein Kinases - metabolism Animal models Animals Aorta Apolipoprotein E Apolipoproteins E - genetics Apolipoproteins E - metabolism Apoptosis Arteriosclerosis Atherosclerosis Atherosclerosis - genetics Atherosclerosis - metabolism Bioinformatics Calciferol Calcification Calcification (ectopic) Deposition Endothelial cells endothelial dysfunction Ferroptosis High fat diet Human Umbilical Vein Endothelial Cells - metabolism Humans Hypertrophy Lipids Lipoproteins Male Metabolic rate Mice Mice, Knockout, ApoE MicroRNAs - metabolism Oxidative stress Receptors Receptors, Calcitriol - genetics Receptors, Calcitriol - metabolism Reporter gene Signal transduction Thorax Transcription Umbilical cables Umbilical vein VDR Vitamin D Vitamin D receptors Vitamins |
| title | Adrenomedullin, transcriptionally regulated by vitamin D receptors, alleviates atherosclerosis in mice through suppressing AMPK‐mediated endothelial ferroptosis |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-13T10%3A02%3A38IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Adrenomedullin,%20transcriptionally%20regulated%20by%20vitamin%20D%20receptors,%20alleviates%20atherosclerosis%20in%20mice%20through%20suppressing%20AMPK%E2%80%90mediated%20endothelial%20ferroptosis&rft.jtitle=Environmental%20toxicology&rft.au=Hu,%20Yanchao&rft.date=2024-01&rft.volume=39&rft.issue=1&rft.spage=199&rft.epage=211&rft.pages=199-211&rft.issn=1520-4081&rft.eissn=1522-7278&rft_id=info:doi/10.1002/tox.23958&rft_dat=%3Cproquest_cross%3E2863297157%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2905509917&rft_id=info:pmid/37688783&rfr_iscdi=true |