<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Xue Y</submitter><funding>Chongqing Medical University</funding><funding>Natural Science Foundation of Chongqing</funding><funding>National Natural Science Foundation of China</funding><pagination>1316</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9715630</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>5(1)</volume><pubmed_abstract>Vascular smooth muscle cells (VSMCs) play a central role in atherosclerosis progression, but the functional changes in VSMCs and the associated cellular crosstalk during atherosclerosis progression remain unknown. Here we show that scRNA-seq analysis of proximal adjacent (PA) and atherosclerotic core (AC) regions of human carotid artery plaques identifies functional alterations in macrophage-like VSMCs, elucidating the main state differences between PA and AC VSMCs. And, IL-1β mediates macrophage-macrophage-like VSMC crosstalk through regulating key transcription factors involved in macrophage-like VSMCs functional alterations during atherosclerosis progression. In vitro assays reveal VSMCs trans-differentiated into a macrophage-like phenotype and then functional alterations in response to macrophage-derived stimuli. IL-1β promots the adhesion, inflammation, and apoptosis of macrophage-like VSMCs in a STAT3 dependent manner. The current findings provide interesting insight into the macrophages-macrophage-like VSMC crosstalk, which would drive functional alterations in the latter cell type through IL-1β/STAT3 axis during atherosclerosis progression.</pubmed_abstract><journal>Communications biology</journal><pubmed_title>Macrophages regulate vascular smooth muscle cell function during atherosclerosis progression through IL-1β/STAT3 signaling.</pubmed_title><pmcid>PMC9715630</pmcid><funding_grant_id>ZHYX202017</funding_grant_id><funding_grant_id>cstc2020jcyj-msxmX1091</funding_grant_id><funding_grant_id>82070238</funding_grant_id><pubmed_authors>Li X</pubmed_authors><pubmed_authors>Shen J</pubmed_authors><pubmed_authors>Hu Y</pubmed_authors><pubmed_authors>Liu L</pubmed_authors><pubmed_authors>Guo Y</pubmed_authors><pubmed_authors>Luo M</pubmed_authors><pubmed_authors>Hu X</pubmed_authors><pubmed_authors>Zhu W</pubmed_authors><pubmed_authors>Huang L</pubmed_authors><pubmed_authors>Luo S</pubmed_authors><pubmed_authors>Xue Y</pubmed_authors><pubmed_authors>Wang L</pubmed_authors></additional><is_claimable>false</is_claimable><name>Macrophages regulate vascular smooth muscle cell function during atherosclerosis progression through IL-1β/STAT3 signaling.</name><description>Vascular smooth muscle cells (VSMCs) play a central role in atherosclerosis progression, but the functional changes in VSMCs and the associated cellular crosstalk during atherosclerosis progression remain unknown. Here we show that scRNA-seq analysis of proximal adjacent (PA) and atherosclerotic core (AC) regions of human carotid artery plaques identifies functional alterations in macrophage-like VSMCs, elucidating the main state differences between PA and AC VSMCs. And, IL-1β mediates macrophage-macrophage-like VSMC crosstalk through regulating key transcription factors involved in macrophage-like VSMCs functional alterations during atherosclerosis progression. In vitro assays reveal VSMCs trans-differentiated into a macrophage-like phenotype and then functional alterations in response to macrophage-derived stimuli. IL-1β promots the adhesion, inflammation, and apoptosis of macrophage-like VSMCs in a STAT3 dependent manner. The current findings provide interesting insight into the macrophages-macrophage-like VSMC crosstalk, which would drive functional alterations in the latter cell type through IL-1β/STAT3 axis during atherosclerosis progression.</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Dec</publication><modification>2025-04-19T03:34:28.625Z</modification><creation>2025-04-07T13:42:31.65Z</creation></dates><accession>S-EPMC9715630</accession><cross_references><pubmed>36456628</pubmed><doi>10.1038/s42003-022-04255-2</doi></cross_references></HashMap>