LKB1 Regulates Inflammation of Fibroblast-like Synoviocytes from Patients with Rheumatoid Arthritis via AMPK-Dependent SLC7A11-NOX4-ROS Signaling

Lee, Ha‐Reum; Yoo, Seung‐Min; Kim, Jinhyun; Kang, Seong Wook

doi:10.3390/cells12091263

Cited by 4 publications

(2 citation statements)

References 46 publications

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“…CX3CR1 [666], CD177 [690], PF4 [691], FFAR2 [692], MPO (myeloperoxidase) [693], F11 [694], S100A8 [695], VEGFD (vascular endothelial growth factor D) [674], IL1A [696], BPI (bactericidal permeability increasing protein) [697], AQP4 [698], BDNF (brain derived neurotrophic factor) [699], CXCL10 [700], RNASE2 [701], FCGR3B [702], S100A9 [703], IL1B [704], CXCR2 [705], GPIHBP1 [294], CD36 [706], TRIB3 [707], PCSK9 [708], FGF2 [709], FASN (fatty acid synthase) [710], PNPLA3 [711], HSPA6 [712], VIP (vasoactive intestinal peptide) [713], TLR3 [683], ADRB1 [328], SPOCK2 [714], TLR8 [715], CCR2 [716], IFIT3 [717], NEK7 [718], TLR7 [687], EFNB2 [719], CAV1 [720], CR1 [721] and AQP5 [722] plays essential roles in viral respiratory diseases. Previous study confirmed that CX3CR1 [723], S100A12 [724], CD177 [725], PF4 [726], MPO (myeloperoxidase) [727], CD5L [728], F11 [729], S100A8 [730], PGLYRP1 [731], GPR15 [732], BPI (bactericidal permeability increasing protein) [733], AQP4 [734], BDNF (brain derived neurotrophic factor) [735], CXCL10 [736], FCGR3B [737], S100A9 [738], IL1B [739], CXCR1 [740], CXCR2 [741], AFF3 [742], WNT3A [743], FCN3 [744], AZGP1 [745], CD36 [746], PCSK9 [747], GPX3 [748], FGF2 [749], SHH (sonic hedgehog signaling molecule) [750], SLC7A11 [751], VIP (vasoactive intestinal peptide) [752], KL (klotho) [753], APOA1 [754], RASGRF1 [75...…”

Section: Discussionmentioning

confidence: 99%

Study on potential differentially expressed genes in idiopathic pulmonary fibrosis by bioinformatics and next generation sequencing data analysis

Vastrad,

Vastrad

2023

Preprint

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Idiopathic pulmonary fibrosis (IPF) is a chronic progressive lung disease with reduced quality of life and earlier mortality, but its pathogenesis and key genes are still unclear. In this investigation, bioinformatics was used to deeply analyze the pathogenesis of IPF and related key genes, so as to investigate the potential molecular pathogenesis of IPF and provide guidance for clinical treatment. Next generation sequencing dataset GSE213001 was obtained from Gene Expression Omnibus (GEO), the differentially expressed genes (DEGs) were identified between IPF and normal control group. The DEGs between IPF and normal control group were screened with the DESeq2 package of R language. The Gene Ontology (GO) and REACTOME pathway enrichment analyses of the DEGs were performed. Using the g:Profiler, the function and pathway enrichment analysis of DEGs were performed. Then, a protein protein interaction (PPI) network was constructed via the Integrated Interactions Database (IID) database. Cytoscape with Network Analyzer was used to identify the hub genes. miRNet and NetworkAnalyst database was used to construct the targeted microRNAs (miRNAs) and transcription factors (TFs) of the hub genes. Finally receiver operating characteristic (ROC) curve analysis was used to validates the hub genes. A total of 958 DEGs were screened out in this study, including 479 up regulated genes and 479 down regulated genes. Most of the DEGs were significantly enriched in response to stimulus, GPCR ligand binding, microtubule-based process and defective GALNT3 causes HFTC. In combination with the results of the PPI network, miRNA-hub gene regulatory network and TF-hub gene regulatory network, hub genes including LRRK2, BMI1, EBP, MNDA, KBTBD7, KRT15, OTX1, TEKT4, SPAG8 and EFHC2 were selected. Our findings will contribute to identification of potential biomarkers and novel strategies for the treatment of IPF, and provide a novel strategy for clinical therapy.

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Section: Discussionmentioning

confidence: 99%

Study on potential differentially expressed genes in idiopathic pulmonary fibrosis by bioinformatics and next generation sequencing data analysis

Vastrad,

Vastrad

2023

Preprint

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“…Excessive ROS are detrimental to non-synovial fibroblasts (N-FLSs); they can promote chondrocyte death by activating the NOX4/p38 MAPK pathway, inducing the expression of matrix metalloproteinases (MMPs), and degrading the cartilage matrix ( 39 ). However, ROS accumulation promotes aberrant proliferation, migration, and the release of inflammatory factors in RA-FLSs, exacerbating arthropathy ( 40 ).Additionally, ROS can promote the receptor activator of nuclear factor-κB ligand (RANKL) expression and induce osteoclast differentiation by activating the Janus kinase (JAK)2/STAT3 pathway, directly or indirectly, through upregulation of hypoxia-inducible factor-1 (HIF-1a) expression ( 41 ). They also participate in key pathological processes, such as angiogenesis and proliferation, by activating the NF-kB pathway to transcribe the vascular endothelial growth factor (VEGF) gene ( 42 ).…”

Section: Ferroptosis In Ramentioning

confidence: 99%

Ferroptosis and endoplasmic reticulum stress in rheumatoid arthritis

Ao,

Hu,

Huang

2024

Front. Immunol.

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Ferroptosis is an iron-dependent mode of cell death distinct from apoptosis and necrosis. Its mechanisms mainly involve disordered iron metabolism, lipid peroxide deposition, and an imbalance of the antioxidant system. The endoplasmic reticulum is an organelle responsible for protein folding, lipid metabolism, and Ca2+ regulation in cells. It can be induced to undergo endoplasmic reticulum stress in response to inflammation, oxidative stress, and hypoxia, thereby regulating intracellular environmental homeostasis through unfolded protein responses. It has been reported that ferroptosis and endoplasmic reticulum stress (ERS) have an interaction pathway and jointly regulate cell survival and death. Both have also been reported separately in rheumatoid arthritis (RA) mechanism studies. However, studies on the correlation between ferroptosis and ERS in RA have not been reported so far. Therefore, this paper reviews the current status of studies and the potential correlation between ferroptosis and ERS in RA, aiming to provide a research reference for developing treatments for RA.

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Contemporary insights and prospects on ferroptosis in rheumatoid arthritis management

Zhao,

Dong,

Hua

et al. 2024

Front. Immunol.

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Rheumatoid arthritis (RA) is a common autoimmune disease characterized primarily by persistent synovial inflammation and joint destruction. In recent years, ferroptosis, as a novel form of cell death, has garnered widespread attention due to its critical role in various diseases. This review explores the potential mechanisms of ferroptosis in RA and its relationship with the pathogenesis of RA, systematically analyzing the regulatory role of ferroptosis in synovial cells, chondrocytes, and immune cells. We emphasize the evaluation of ferroptosis-related pathways and their potential as therapeutic targets, including the development and application of inhibitors and activators. Although ferroptosis shows some promise in RA treatment, its dual role and safety issues in clinical application still require in-depth study. Future research should focus on elucidating the specific mechanisms of ferroptosis in RA pathology and developing more effective and safer therapeutic strategies to provide new treatment options for RA patients.

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LKB1 Regulates Inflammation of Fibroblast-like Synoviocytes from Patients with Rheumatoid Arthritis via AMPK-Dependent SLC7A11-NOX4-ROS Signaling

Cited by 4 publications

References 46 publications

Study on potential differentially expressed genes in idiopathic pulmonary fibrosis by bioinformatics and next generation sequencing data analysis

Study on potential differentially expressed genes in idiopathic pulmonary fibrosis by bioinformatics and next generation sequencing data analysis

Ferroptosis and endoplasmic reticulum stress in rheumatoid arthritis

Contemporary insights and prospects on ferroptosis in rheumatoid arthritis management

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