ArticleLung2024
Neutralization of CX3CL1 Attenuates TGF-β-Induced Fibroblast Differentiation Through NF-κB Activation and Mitochondrial Dysfunction in Airway Fibrosis.
Article in Lung, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- EpCAM aptamer modified carbon@manganese dioxide nanoflower for synergistic drug-nanozyme allergic rhinitis treatment.Materials today. Bio · 2026Article
- DCLK1 mediates airway epithelial barrier disruption through NF-κB activation in severe asthma.Molecular medicine (Cambridge, Mass.) · 2026Article
- FNDC5/Irisin Attenuates TGF-β-induced Fibroblast Differentiation Via AMPK/Nrf2 Signaling and Mitochondrial Stabilization in Subepithelial Fibrosis.Inflammation · 2026Article
- An injectable self-healing curcumin-sustained-release hydrogel for lower limb ischemia via autophagy inhibition byRegenerative biomaterials · 2026Article
- LA-peptide Hydrogel-Regulation of macrophage and fibroblast fates and their crosstalk via attenuating TGF-β to promote scarless wound healing.Bioactive materials · 2025Article
- LUNG Year in Review: 2024.Lung · 2025Article
- Mechanisms of prostatic inflammation-mediated male lower urinary tract symptoms.American journal of clinical and experimental urology · 2025Review
- Mechanisms underlying the involvement of peritoneal macrophages in the pathogenesis and novel therapeutic strategies for dialysis-induced peritoneal fibrosis.Frontiers in immunology · 2024Review
- Roles of Exosomal miRNAs in Asthma: Mechanisms and Applications.Journal of asthma and allergy · 2024Review
- Modified Wen Luo Tong Alleviated Chemotherapy-Induced Peripheral Neuropathy via Regulating the CX3CL1/CX3CR1 Axis Through Inhibiting NF-κB and STAT3 Pathways.Integrative cancer therapiesArticle
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11 authors.
Funding
Abstract
backgroundSevere asthma, characterized by inflammation and airway remodeling, involves fibroblast differentiation into myofibroblasts expressing α-SMA. This process leads to the production of fibronectin and connective tissue growth factor (CTGF), driven by factors such as transforming growth factor (TGF)-β. Furthermore, the persistent presence of myofibroblasts is associated with resistance to apoptosis and mitochondrial dysfunction. The chemokine (C-X3-C motif) ligand 1 (CX3CL1) plays a role in tissue fibrosis. However, it is currently unknown whether neutralization of CX3CL1 decreases TGF-β-induced fibroblast differentiation and mitochondrial dysfunction in normal human lung fibroblasts (NHLFs).
methodsCX3CL1/C-X3-C motif chemokine receptor 1 (CX3CR1), CX3CL1 was analyzed by immunofluorescence (IF) or immunohistochemical (IHC) staining of ovalbumin-challenged mice. CX3CL1 release was detected by ELISA. TGF-β-induced CTGF, fibronectin, and α-SMA expression were evaluated in NHLFs following neutralization of CX3CL1 (TP213) treatment for the indicated times by Western blotting or IF staining. Mitochondrion function was detected by a JC-1 assay and seahorse assay. Cell apoptosis was observed by a terminal uridine nick-end labeling (TUNEL) assay.
resultsAn increase in CX3CL1 expression was observed in lung tissues from mice with ovalbumin-induced asthma by IF staining. CX3CR1 was increased in the subepithelial layer of the airway by IHC staining. Moreover, CX3CR1 small interfering (si)RNA downregulated TGF-β-induced CTGF and fibronectin expression in NHLFs. CX3CL1 induced CTGF and fibronectin expression in NHLFs. TGF-β-induced CX3CL1 secretion from NHLFs. Furthermore, TP213 decreased TGF-β-induced CTGF, fibronectin, and α-SMA expression in NHLFs. Mitochondrion-related differentially expressed genes (DEGs) were examined after CX3CL1 neutralization in TGF-β-treated NHLFs. TP213 alleviated TGF-β-induced mitochondrial dysfunction and apoptosis resistance in NHLFs. CX3CL1 induced p65, IκBα, and IKKα phosphorylation in a time-dependent manner. Furthermore, CX3CL1-induced fibronectin expression and JC-1 monomer were decreased by p65 siRNA. TP213 reduced TGF-β-induced p65 and α-SMA expression in NHLFs.
conclusionsThese findings suggest that neutralizing CX3CL1 attenuates lung fibroblast activation and mitochondrial dysfunction. Understanding the impacts of CX3CL1 neutralization on fibroblast mitochondrial function could contribute to the development of therapeutic strategies for managing airway remodeling in severe asthma.
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