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SFRP1 负向调节类风湿关节炎成纤维样滑膜细胞焦亡:综述。

SFRP1 Negatively Modulates Pyroptosis of Fibroblast-Like Synoviocytes in Rheumatoid Arthritis: A Review.

机构信息

Guanghua Clinical Medical College, Shanghai University of Traditional Chinese Medicine, Shanghai, China.

Department of Rheumatology, Shanghai Guanghua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China.

出版信息

Front Immunol. 2022 Jun 20;13:903475. doi: 10.3389/fimmu.2022.903475. eCollection 2022.

DOI:10.3389/fimmu.2022.903475
PMID:35795672
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9251540/
Abstract

Secreted frizzled-related protein 1 (SFRP1) is a member of secretory glycoprotein SFRP family. As a primitive gene regulating cell growth, development and transformation, SFRP1 is widely expressed in human cells, including various cancer cells and fibroblast-like synoviocytes (FLS) of rheumatoid arthritis (RA). Deletion or silencing of SFRP1 involves epigenetic and other mechanisms, and participates in biological behaviors such as cell proliferation, migration and cell pyroptosis, which leads to disease progression and poor prognosis. In this review, we discuss the role of SFRP1 in the pathogenesis of RA-FLS and summarize different experimental platforms and recent research results. These are helpful for understanding the biological characteristics of SFRP1 in RA, especially the mechanism by which SFRP1 regulates RA-FLS pyroptosis through Wnt/β-catenin and Notch signaling pathways. In addition, the epigenetic regulation of SFRP1 in RA-FLS is emphasized, which may be considered as a promising biomarker and therapeutic target of RA.

摘要

分泌卷曲相关蛋白 1(SFRP1)是分泌糖蛋白 SFRP 家族的一员。作为一个调节细胞生长、发育和转化的原始基因,SFRP1 在人类细胞中广泛表达,包括各种癌细胞和类风湿关节炎(RA)的成纤维样滑膜细胞(FLS)。SFRP1 的缺失或沉默涉及表观遗传等机制,并参与细胞增殖、迁移和细胞焦亡等生物学行为,导致疾病进展和预后不良。在这篇综述中,我们讨论了 SFRP1 在 RA-FLS 发病机制中的作用,并总结了不同的实验平台和最近的研究结果。这些有助于了解 SFRP1 在 RA 中的生物学特性,特别是 SFRP1 通过 Wnt/β-catenin 和 Notch 信号通路调节 RA-FLS 焦亡的机制。此外,还强调了 SFRP1 在 RA-FLS 中的表观遗传调控,这可能被认为是 RA 的有前途的生物标志物和治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9f0/9251540/9837cb7fe221/fimmu-13-903475-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9f0/9251540/d22210cfd123/fimmu-13-903475-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9f0/9251540/292e4f4851af/fimmu-13-903475-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9f0/9251540/d529ec7ec2de/fimmu-13-903475-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9f0/9251540/9837cb7fe221/fimmu-13-903475-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9f0/9251540/d22210cfd123/fimmu-13-903475-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9f0/9251540/292e4f4851af/fimmu-13-903475-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9f0/9251540/d529ec7ec2de/fimmu-13-903475-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9f0/9251540/9837cb7fe221/fimmu-13-903475-g004.jpg

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