ArticleCell & bioscience2019
CXCR4 knockdown prevents inflammatory cytokine expression in macrophages by suppressing activation of MAPK and NF-κB signaling pathways.
Article in Cell & bioscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 74 citations in OpenAlex.
- A randomized, placebo-controlled trial of the BTK inhibitor zanubrutinib in hospitalized patients with COVID-19 respiratory distress: immune biomarker and clinical findings.Frontiers in immunology · 2024Trial
- Comprehensive characterization of the inflammatory ecosystems in immunotherapy-induced adverse events versus chronic inflammatory diseases.Journal for immunotherapy of cancer · 2026Article
- Inhibition of Cxcr4 chemokine receptor signaling improves habituation learning in a zebrafish model of neurofibromatosis.Disease models & mechanisms · 2026Article
- G-CSF promotes H3K27ac-modified KLF5 to activate CXCR4 expression and drive colon cancer growth and metastasis.European journal of medical research · 2026Article
- Neuroprotective effects of telmisartan in a harmaline-induced model of essential tremor: modulation of the renin-angiotensin system and inflammatory pathways.Frontiers in pharmacology · 2026Article
- CXCR4 inhibition alleviates prostatic inflammation and pelvic pain via suppressing Th17 cell differentiation and oxidative stress in EAP mice.International journal of biological sciences · 2026Article
- Deciphering the Interlinked CXCR4-Mediated Feedback Loop Among Signaling Pathways in Diabetic Wound Healing.Current diabetes reviews · 2026Review
- The CXCL12/CXCR4 Axis in Sepsis-Induced Acute Lung Injury: Mechanisms and Therapeutic Potential.Current issues in molecular biology · 2025Review
- Transcriptomic profile of TiOArchives of toxicology · 2025Article
- Diurnally-Regulated Corticosterone and Melatonin Inversely Control Endotoxin-Induced Acute Immune Responses.European journal of immunology · 2025Article
- scRNA-seq reveals persistent aberrant differentiation of nasal epithelium driven by TNFα and TGFβ in post-COVID syndrome.Nature communications · 2025Article
- Unique transcriptomic responses of rat and human alveolar macrophages in an in vitro model of overload with TiOParticle and fibre toxicology · 2025Article
- The regulatory role of immune microenvironment-related cells and pathways in the pathogenesis of keloids.Frontiers in immunology · 2025Review
- Mass spectrometry-based proteomic exploration of diverse murine macrophage cellular models.Life science alliance · 2025Article
- Second Generation I-Body AD-214 Attenuates Unilateral Ureteral Obstruction (UUO)-Induced Kidney Fibrosis Through Inhibiting Leukocyte Infiltration and Macrophage Migration.International journal of molecular sciences · 2024Article
- Use of Extracellular Monomeric Ubiquitin as a Therapeutic Option for Major Depressive Disorder.Pharmaceuticals (Basel, Switzerland) · 2024Article
- A simultaneous knockout knockin genome editing strategy in HSPCs potently inhibits CCR5- and CXCR4-tropic HIV-1 infection.Cell stem cell · 2024Article
- Migratory mode transition of astrocyte progenitors in the cerebral cortex: an intrinsic or extrinsic cell process?Neural regeneration research · 2024Article
- The complex nature of CXCR4 mutations in WHIM syndrome.Frontiers in immunology · 2024Review
- Epigenetic regulation of macrophage activation in chronic obstructive pulmonary disease.Frontiers in immunology · 2024Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundRecent evidence has shown that C-X-C chemokine receptor type 4 (CXCR4) plays a crucial role in acute lung injury (ALI). Macrophages are key factors in the pathogenesis of ALI. The aim of this study was to investigate the role of CXCR4 in macrophages after lipopolysaccharide (LPS) stimulation and confirm that CXCR4 knockdown can inhibit inflammatory cytokines by suppressing mitogen-activated protein kinase (MAPK) and nuclear factor-κB (NF-κB) signaling pathway activation.
resultsIn this study, we found that CXCR4 expression in lung tissue of ALI was significantly increased using immunofluorescence. We also found that the expression of CXCR4 in macrophages sorted from bronchoalveolar lavage fluid (BALF) of ALI was obviously upregulated through RT-qPCR. After CXCR4 knockdown using siRNA, we found that the expression of interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) was obviously down regulated in macrophages. Additionally, the phosphorylation of p38, Erk, and p65 was significantly decreased after CXCR4 knockdown through western blotting.
conclusionsTaken together, the present study suggests that CXCR4 knockdown may inhibit inflammatory cytokine expression in macrophages by suppressing MAPK and NF-κB signaling pathway activation. Therefore, CXCR4 knockdown may have potential clinical value in treating ALI.
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