{"title":"Single-cell analysis identified key macrophage subpopulations associated with atherosclerosis.","authors":"Zhenzhen Zhao, Yuelong Qin, Rui Wu, Wenwu Li, Yujiang Dong","doi":"10.1515/med-2024-1088","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Atherosclerosis is a lipid-driven inflammatory disease characterized by plaque formation in major arteries. These plaques contain lipid-rich macrophages that accumulate through monocyte recruitment, local macrophage differentiation, and proliferation.</p><p><strong>Objective: </strong>We identify the macrophage subsets that are closely related to atherosclerosis and reveal the key pathways in the progression of atherosclerotic disease.</p><p><strong>Materials and methods: </strong>In this study, we characterize the single-cell landscape of atherosclerosis, identifying macrophage subsets closely related to the disease and revealing key pathways in its progression. Using analytical methods like CytoTRACE, Monocle2, Slingshot, and CellChat, we study macrophage differentiation and infer cell trajectory.</p><p><strong>Results: </strong>The 8,417 macrophages were divided into six subtypes, macrophages: C0 C1QC+ macrophages, C1 SPP1+ macrophages, C2 FCN1+ macrophages, C3 IGKC+ macrophages, C4 FCER1A+ macrophages, C5CALD1+ macrophages. The results of gene set enrichment analysis, Monocle2, and Slingshot suggest that C2 FCN1+ macrophages may play an important role in the progression of atherosclerosis. C2 FCN1+ macrophages interact with endothelial cells via CCL, CXCL, APP, and other pathways to regulate the progression of atherosclerosis.</p><p><strong>Conclusion: </strong>We identify a key macrophage subgroup (C2 FCN1+ macrophages) associated with atherosclerosis, which interacts with endothelial cells via CCL, CXCL, APP, and other pathways to regulate disease progression.</p>","PeriodicalId":19715,"journal":{"name":"Open Medicine","volume":"19 1","pages":"20241088"},"PeriodicalIF":1.7000,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11669903/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Open Medicine","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1515/med-2024-1088","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/1/1 0:00:00","PubModel":"eCollection","JCR":"Q2","JCRName":"MEDICINE, GENERAL & INTERNAL","Score":null,"Total":0}
引用次数: 0
Abstract
Background: Atherosclerosis is a lipid-driven inflammatory disease characterized by plaque formation in major arteries. These plaques contain lipid-rich macrophages that accumulate through monocyte recruitment, local macrophage differentiation, and proliferation.
Objective: We identify the macrophage subsets that are closely related to atherosclerosis and reveal the key pathways in the progression of atherosclerotic disease.
Materials and methods: In this study, we characterize the single-cell landscape of atherosclerosis, identifying macrophage subsets closely related to the disease and revealing key pathways in its progression. Using analytical methods like CytoTRACE, Monocle2, Slingshot, and CellChat, we study macrophage differentiation and infer cell trajectory.
Results: The 8,417 macrophages were divided into six subtypes, macrophages: C0 C1QC+ macrophages, C1 SPP1+ macrophages, C2 FCN1+ macrophages, C3 IGKC+ macrophages, C4 FCER1A+ macrophages, C5CALD1+ macrophages. The results of gene set enrichment analysis, Monocle2, and Slingshot suggest that C2 FCN1+ macrophages may play an important role in the progression of atherosclerosis. C2 FCN1+ macrophages interact with endothelial cells via CCL, CXCL, APP, and other pathways to regulate the progression of atherosclerosis.
Conclusion: We identify a key macrophage subgroup (C2 FCN1+ macrophages) associated with atherosclerosis, which interacts with endothelial cells via CCL, CXCL, APP, and other pathways to regulate disease progression.
期刊介绍:
Open Medicine is an open access journal that provides users with free, instant, and continued access to all content worldwide. The primary goal of the journal has always been a focus on maintaining the high quality of its published content. Its mission is to facilitate the exchange of ideas between medical science researchers from different countries. Papers connected to all fields of medicine and public health are welcomed. Open Medicine accepts submissions of research articles, reviews, case reports, letters to editor and book reviews.