<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>23(4)</volume><submitter>Jia J</submitter><pubmed_abstract>The vitamin D receptor (VDR) may regulate blood pressure via multiple pathways. The present study investigated the underlying mechanism by which &lt;i>VDR&lt;/i> deficiency increases blood pressure. A total of 16 8-week-old male littermate mice were randomly divided into the &lt;i>VDR&lt;/i> knockout and wild-type groups (&lt;i>VDR&lt;sup>-/-&lt;/sup>&lt;/i> and &lt;i>VDR&lt;sup>+/+&lt;/sup>&lt;/i> , respectively). Blood pressure was measured using a four-channel PowerLab data acquisition and ADI software analysis system. After euthanasia, vascular smooth muscle cells (VSMCs) were isolated from the &lt;i>VDR&lt;sup>-/-&lt;/sup>&lt;/i> and &lt;i>VDR&lt;sup>+/+&lt;/sup>&lt;/i> mice. Oxidative stress, renin-angiotensin system (&lt;i>RAS&lt;/i>) activation and autophagy markers were measured in the isolated VSMCs using reverse transcription-quantitative PCR (RT-qPCR), western blotting and transmission electron microscopy (TEM) assays. Mean systolic pressure was significantly higher in the &lt;i>VDR&lt;sup>-/-&lt;/sup>&lt;/i> mice compared with the &lt;i>VDR&lt;sup>+/+&lt;/sup>&lt;/i> mice. RT-qPCR and western blotting analyses indicated that RAS markers (angiotensin II and II type 1 receptor) were significantly upregulated, oxidative stress was increased (evidenced by reduced superoxide dismutase and peroxiredoxin-4) and autophagy was activated (upregulation of autophagy related protein 7, Beclin 1 and microtubule-associated proteins 1A/1B light chain 3A) in the &lt;i>VDR&lt;sup>-/-&lt;/sup>&lt;/i> VSMCs compared with the &lt;i>VDR&lt;sup>+/+&lt;/sup>&lt;/i> VSMCs. TEM demonstrated that there were more autophagy bodies in the &lt;i>VDR&lt;sup>-/-&lt;/sup>&lt;/i> VSMCs compared with the &lt;i>VDR&lt;sup>+/+&lt;/sup>&lt;/i> VSMCs. In conclusion, &lt;i>VDR&lt;/i> deficiency was associated with high blood pressure. The mechanism underlying the increase in blood pressure caused by &lt;i>VDR&lt;/i> deficiency may involve activation of the RAS, as well as increased oxidative stress and autophagy of VSMCs.</pubmed_abstract><journal>Experimental and therapeutic medicine</journal><pagination>314</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8943549</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Vitamin D receptor deficiency increases systolic blood pressure by upregulating the renin-angiotensin system and autophagy.</pubmed_title><pmcid>PMC8943549</pmcid><pubmed_authors>Tian Z</pubmed_authors><pubmed_authors>Liu J</pubmed_authors><pubmed_authors>Tao X</pubmed_authors><pubmed_authors>Ye X</pubmed_authors><pubmed_authors>Jia J</pubmed_authors><pubmed_authors>Zhan Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>Vitamin D receptor deficiency increases systolic blood pressure by upregulating the renin-angiotensin system and autophagy.</name><description>The vitamin D receptor (VDR) may regulate blood pressure via multiple pathways. The present study investigated the underlying mechanism by which &lt;i>VDR&lt;/i> deficiency increases blood pressure. A total of 16 8-week-old male littermate mice were randomly divided into the &lt;i>VDR&lt;/i> knockout and wild-type groups (&lt;i>VDR&lt;sup>-/-&lt;/sup>&lt;/i> and &lt;i>VDR&lt;sup>+/+&lt;/sup>&lt;/i> , respectively). Blood pressure was measured using a four-channel PowerLab data acquisition and ADI software analysis system. After euthanasia, vascular smooth muscle cells (VSMCs) were isolated from the &lt;i>VDR&lt;sup>-/-&lt;/sup>&lt;/i> and &lt;i>VDR&lt;sup>+/+&lt;/sup>&lt;/i> mice. Oxidative stress, renin-angiotensin system (&lt;i>RAS&lt;/i>) activation and autophagy markers were measured in the isolated VSMCs using reverse transcription-quantitative PCR (RT-qPCR), western blotting and transmission electron microscopy (TEM) assays. Mean systolic pressure was significantly higher in the &lt;i>VDR&lt;sup>-/-&lt;/sup>&lt;/i> mice compared with the &lt;i>VDR&lt;sup>+/+&lt;/sup>&lt;/i> mice. RT-qPCR and western blotting analyses indicated that RAS markers (angiotensin II and II type 1 receptor) were significantly upregulated, oxidative stress was increased (evidenced by reduced superoxide dismutase and peroxiredoxin-4) and autophagy was activated (upregulation of autophagy related protein 7, Beclin 1 and microtubule-associated proteins 1A/1B light chain 3A) in the &lt;i>VDR&lt;sup>-/-&lt;/sup>&lt;/i> VSMCs compared with the &lt;i>VDR&lt;sup>+/+&lt;/sup>&lt;/i> VSMCs. TEM demonstrated that there were more autophagy bodies in the &lt;i>VDR&lt;sup>-/-&lt;/sup>&lt;/i> VSMCs compared with the &lt;i>VDR&lt;sup>+/+&lt;/sup>&lt;/i> VSMCs. In conclusion, &lt;i>VDR&lt;/i> deficiency was associated with high blood pressure. The mechanism underlying the increase in blood pressure caused by &lt;i>VDR&lt;/i> deficiency may involve activation of the RAS, as well as increased oxidative stress and autophagy of VSMCs.</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Apr</publication><modification>2026-05-31T01:05:11.026Z</modification><creation>2025-04-04T11:31:36.278Z</creation></dates><accession>S-EPMC8943549</accession><cross_references><pubmed>35369533</pubmed><doi>10.3892/etm.2022.11243</doi></cross_references></HashMap>