Destructive Roles of Fibroblast-like Synoviocytes in Chronic Inflammation and Joint Damage in Rheumatoid Arthritis
- PMID: 33113036
- DOI: 10.1007/s10753-020-01371-1
Destructive Roles of Fibroblast-like Synoviocytes in Chronic Inflammation and Joint Damage in Rheumatoid Arthritis
Erratum in
-
Correction to: Destructive Roles of Fibroblast-Like Synoviocytes in Chronic Inflammation and Joint Damage in Rheumatoid Arthritis.Inflammation. 2021 Apr;44(2):480. doi: 10.1007/s10753-020-01402-x. Inflammation. 2021. PMID: 33319320 No abstract available.
Abstract
Fibroblast-like synoviocytes (FLSs) are important non-immune cells located mostly in the inner layer of the synovium. Indeed, these cells are specialized mesenchymal cells, implicated in collagen homeostasis of the articular joint and provide extracellular matrix (ECM) materials for cartilage and contribute to joint destruction via multiple mechanisms. RA FLS interactions with immune and non-immune cells lead to the development and organization of tertiary structures such as ectopic lymphoid-like structures (ELSs), tertiary lymphoid organs (TLOs), and secretion of proinflammatory cytokines. The interaction of RA FLS cells with immune and non-immune cells leads to stimulation and activation of effector immune cells. Pathological role of RA FLS cells has been reported for many years, while molecular and cellular mechanisms are not completely understood yet. In this review, we tried to summarize the latest findings about the role of FLS cells in ELS formation, joint destruction, interactions with immune and non-immune cells, as well as potential therapeutic options in rheumatoid arthritis (RA) treatment. Our study revealed data about interactions between RA FLS and immune/non-immune cells as well as the role of RA FLS cells in joint damage, ELS formation, and neoangiogenesis, which provide useful information for developing new approaches for RA treatment.
Keywords: Immune and non-immune cells; ectopic lymphoid-like structures (ELSs); fibroblast-like synoviocytes (FLSs); rheumatoid arthritis (RA).
Similar articles
-
Regulation of Immune Responses and Chronic Inflammation by Fibroblast-Like Synoviocytes.Front Immunol. 2019 Jun 19;10:1395. doi: 10.3389/fimmu.2019.01395. eCollection 2019. Front Immunol. 2019. PMID: 31275325 Free PMC article. Review.
-
TL1A/TNFR2-mediated mitochondrial dysfunction of fibroblast-like synoviocytes increases inflammatory response in patients with rheumatoid arthritis via reactive oxygen species generation.FEBS J. 2020 Jul;287(14):3088-3104. doi: 10.1111/febs.15181. Epub 2020 Jan 17. FEBS J. 2020. PMID: 31953914
-
DDR2-CYR61-MMP1 Signaling Pathway Promotes Bone Erosion in Rheumatoid Arthritis Through Regulating Migration and Invasion of Fibroblast-Like Synoviocytes.J Bone Miner Res. 2017 Feb;32(2):407-418. doi: 10.1002/jbmr.2993. Epub 2016 Nov 3. J Bone Miner Res. 2017. PMID: 27653023
-
Restoring synovial homeostasis in rheumatoid arthritis by targeting fibroblast-like synoviocytes.Nat Rev Rheumatol. 2020 Jun;16(6):316-333. doi: 10.1038/s41584-020-0413-5. Epub 2020 May 11. Nat Rev Rheumatol. 2020. PMID: 32393826 Free PMC article. Review.
-
IL-17-mediated mitochondrial dysfunction impairs apoptosis in rheumatoid arthritis synovial fibroblasts through activation of autophagy.Cell Death Dis. 2017 Jan 19;8(1):e2565. doi: 10.1038/cddis.2016.490. Cell Death Dis. 2017. PMID: 28102843 Free PMC article.
Cited by
-
Exploring the mechanism of Celastrol in the treatment of rheumatoid arthritis based on systems pharmacology and multi-omics.Sci Rep. 2024 Jan 18;14(1):1604. doi: 10.1038/s41598-023-48248-5. Sci Rep. 2024. PMID: 38238321 Free PMC article.
-
Gene Network Analyses Identify Co-regulated Transcription Factors and BACH1 as a Key Driver in Rheumatoid Arthritis Fibroblast-like Synoviocytes.bioRxiv [Preprint]. 2024 Jan 8:2023.12.28.573506. doi: 10.1101/2023.12.28.573506. bioRxiv. 2024. PMID: 38234777 Free PMC article. Preprint.
-
Quercetin is a Potential Therapy for Rheumatoid Arthritis via Targeting Caspase-8 Through Ferroptosis and Pyroptosis.J Inflamm Res. 2023 Dec 1;16:5729-5754. doi: 10.2147/JIR.S439494. eCollection 2023. J Inflamm Res. 2023. PMID: 38059150 Free PMC article.
-
Ferroptosis as an emerging target in rheumatoid arthritis.Front Immunol. 2023 Oct 19;14:1260839. doi: 10.3389/fimmu.2023.1260839. eCollection 2023. Front Immunol. 2023. PMID: 37928554 Free PMC article. Review.
-
Rheumatoid arthritis: the old issue, the new therapeutic approach.Stem Cell Res Ther. 2023 Sep 23;14(1):268. doi: 10.1186/s13287-023-03473-7. Stem Cell Res Ther. 2023. PMID: 37741991 Free PMC article. Review.
References
-
- Karami J, Masoumi M, Khorramdelazad H, Bashiri H, Darvishi P, Sereshki HA et al. 2020. Role of autophagy in the pathogenesis of rheumatoid arthritis: latest evidence and therapeutic approaches. Life Sciences. 117734.
-
- Fang, Q., C. Zhou, and K.S. Nandakumar. 2020. Molecular and cellular pathways contributing to joint damage in rheumatoid arthritis. Mediators of Inflammation 2020: 1–20.
-
- McInnes, I.B., and G. Schett. 2011. The pathogenesis of rheumatoid arthritis. New England Journal of Medicine 365 (23): 2205–2219.
-
- Gregersen, P.K., J. Silver, and R.J. Winchester. 1987. The shared epitope hypothesis. An approach to understanding the molecular genetics of susceptibility to rheumatoid arthritis. Arthritis & Rheumatism: Official Journal of the American College of Rheumatology. 30 (11): 1205–1213.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Medical
