ArticleCell communication and signaling : CCS2024
CXCR4 regulates macrophage M1 polarization by altering glycolysis to promote prostate fibrosis.
Article in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
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Who cites it
27 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Vascular Immunometabolism in Atherosclerosis: Emerging Roles of Glycometabolic Reprogramming in Immune and Vascular Cells.Cardiovascular drugs and therapy · 2026Pooled it
- The Metabolic Reprogramming Mechanism of Astragalus Polysaccharide-Induced Immune Memory in HD11 Cells: Integrated Analysis Based on Glycolysis and the TLR2/mTOR Pathway.Poultry science · 2026Article
- Mechanism of Kushen Tongguan Pill on benign prostatic hyperplasia: roles of TLR4/NF-κB pathway and macrophage M1 polarization.Journal of molecular histology · 2026Article
- Development and evaluation of a novel experimental autoimmune prostatitis model induced by a prostate-specific antigen mixture in rats.Biochemistry and biophysics reports · 2026Article
- Spatially resolved fetal and maternal cell contributions to severe preeclampsia across gestation.Science advances · 2026Article
- Article
- Multi-omic insight into the molecular networks of macrophage polarization in the pathogenesis of atrial fibrillation.Journal of cardiothoracic surgery · 2026Article
- A bioinformatics analysis of the PIEZO channel interaction network and the genes related to glycometabolic reprogramming and mitochondrial oxidative phosphorylation in the progression of prostatic hyperplasia.Translational andrology and urology · 2026Article
- METTL3-mediated m6A modification of CXCR4 drives M2 macrophage polarization and suppresses anti-tumor immunity in esophageal cancer.Journal of clinical biochemistry and nutrition · 2026Article
- Epithelial redox stress programs macrophage immunometabolism through a ZNF24-MIF-NF-κB pathway in chronic nonbacterial prostatitis.Redox biology · 2026Article
- Leonurine Mitigates Experimental Autoimmune Prostatitis by Modulating Macrophage M1 Polarization Through the TLR4/NF-κB Signaling Pathway.Inflammation · 2026Article
- UHPLC-Q-Orbitrap-HRMS-Based Multilayer Mapping of the Pharmacodynamic Substance Basis and Mechanistic Landscape of Maizibizi Wan in Chronic Nonbacterial Prostatitis Therapy.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Immune remodeling in chronic prostatitis: from microenvironment imbalance to targeted therapy.Frontiers in molecular biosciences · 2026Article
- Immune-cell imbalance and immunometabolic reprogramming in chronic prostatitis/chronic pelvic pain syndrome.Frontiers in immunology · 2026Review
- Biomechanical signaling of cytoskeleton and membrane reorganization in tumor immune chemotactic migration.Theranostics · 2026Review
- Macrophage immunometabolism in osteoporosis: an emerging regulatory axis linking metabolic-polarization coupling to therapeutic targets.Frontiers in immunology · 2026Review
- Metabolic licensing and restriction of innate immunity in the tumor microenvironment.Frontiers in immunology · 2026Review
- Enhanced CHI3L1 promotes macrophage activation in persistent inflammatory events of ulcerative interstitial cystitis.Frontiers in immunology · 2026Article
- Immunomodulatory Mechanisms of Chronic Wound Healing: Translational and Clinical Relevance.MedComm · 2025Review
- Mechanisms and etiology of male health disorders: hormones, cancer, and fertility.Cell communication and signaling : CCS · 2025Article
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundC-X-C receptor 4(CXCR4) is widely considered to be a highly conserved G protein-coupled receptor, widely involved in the pathophysiological processes in the human body, including fibrosis. However, its role in regulating macrophage-related inflammation in the fibrotic process of prostatitis has not been confirmed. Here, we aim to describe the role of CXCR4 in modulating macrophage M1 polarization through glycolysis in the development of prostatitis fibrosis.
methodsUse inducible experimental chronic prostatitis as a model of prostatic fibrosis. Reduce CXCR4 expression in immortalized bone marrow-derived macrophages using lentivirus. In the fibrotic mouse model, use adenovirus carrying CXCR4 agonists to detect the silencing of CXCR4 and assess the in vivo effects.
resultsIn this study, we demonstrated that reducing CXCR4 expression during LPS treatment of macrophages can alleviate M1 polarization. Silencing CXCR4 can inhibit glycolytic metabolism, enhance mitochondrial function, and promote macrophage transition from M1 to M2. Additionally, in vivo functional experiments using AAV carrying CXCR4 showed that blocking CXCR4 in experimental autoimmune prostatitis (EAP) can alleviate inflammation and experimental prostate fibrosis development. Mechanistically, CXCR4, a chemokine receptor, when silenced, weakens the PI3K/AKT/mTOR pathway as its downstream signal, reducing c-MYC expression. PFKFB3, a key enzyme involved in glucose metabolism, is a target gene of c-MYC, thus impacting macrophage polarization and glycolytic metabolism processes.
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