Multi-Omics Exploration of the Role of PTGS2 as a Hub Gene in Ferroptosis Within the Artery of Takayasu Arteritis.

IF 4.2 2区医学 Q2 IMMUNOLOGY

Journal of Inflammation Research Pub Date : 2024-11-19 eCollection Date: 2024-01-01 DOI:10.2147/JIR.S478413

Qing Gao, Shang Gao, Haiyang Li, Zuoguan Chen, Ran Zhang, Yongjun Li, Hongjia Zhang

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引用次数: 0

Abstract

Introduction: Takayasu arteritis (TAK) is an autoimmune disease affecting the aorta and its branches. Despite anti-inflammatory treatments, some patients require surgical vascular reconstruction due to rapid disease progression. The mechanisms behind persistent inflammation are unclear due to a lack of arterial samples. This study explores ferroptosis in TAK using high-throughput and single-cell transcriptomics.

Methods: Transcriptomic data were collected from 8 TAK patients (2 for single cell RNA-seq and 6 for bulk RNA-seq) and 8 renal transplant donors, with single-cell data from 3 public carotid artery samples for control. Bioinformatic analysis was performed to identify ferroptosis-related genes in inflamed arteries.

Results: We identified 1526 differentially expressed genes and 46 ferroptosis-related genes, with 6 genes including PTGS2 and HIF1A as hub genes. Single-cell analysis of 27,828 cells revealed increased M1-like macrophages, with PTGS2 highly expressed in these cells. Enrichment analysis indicated NF-κB signal pathway involvement.

Conclusion: PTGS2 is a core ferroptosis-related gene in TAK vascular inflammation, highly expressed in M1-like macrophages, potentially upregulated via the IL1B-NF-κB pathway.

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多指标探究 PTGS2 作为高安动脉炎动脉内铁蛋白沉积的枢纽基因的作用

导言高安动脉炎（TAK）是一种影响主动脉及其分支的自身免疫性疾病。尽管采取了抗炎治疗，但由于疾病进展迅速，一些患者仍需要进行外科血管重建。由于缺乏动脉样本，持续炎症背后的机制尚不清楚。本研究利用高通量和单细胞转录组学探讨了 TAK 中的铁蛋白沉积：方法：从8名TAK患者（2名单细胞RNA-seq和6名批量RNA-seq）和8名肾移植供体中收集转录组数据，并从3个公共颈动脉样本中收集单细胞数据作为对照。我们进行了生物信息学分析，以确定炎症动脉中与铁突变相关的基因：结果：我们发现了1526个差异表达基因和46个铁变态反应相关基因，其中包括PTGS2和HIF1A在内的6个基因是枢纽基因。对 27828 个细胞进行的单细胞分析显示，M1 样巨噬细胞增加，PTGS2 在这些细胞中高表达。富集分析表明NF-κB信号通路参与其中：结论：PTGS2是TAK血管炎症中与铁蛋白沉积相关的核心基因，在M1样巨噬细胞中高表达，可能通过IL1B-NF-κB通路上调。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Journal of Inflammation Research Immunology and Microbiology-Immunology

CiteScore

6.10

自引率

2.20%

发文量

658

审稿时长

16 weeks

期刊介绍： An international, peer-reviewed, open access, online journal that welcomes laboratory and clinical findings on the molecular basis, cell biology and pharmacology of inflammation.