ArticleFrontiers in immunology2025
Targeted inhibitors of S100A9 alleviate chronic pancreatitis by inhibiting M2 macrophage polarization via the TAOK3-JNK signaling pathway.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Thousand-And-One Kinase 3 in Pancreatic Ductal Adenocarcinoma Stemness, Microenvironment and Therapy Resistance.International journal of molecular sciences · 2026Review
- Quercetin Inhibits Orthodontic Tooth Movement-Associated Periodontitis by Regulating Macrophage Aerobic Glycolysis Through the IL-17/Hippo/YAP Axis.Clinical and experimental dental research · 2026Article
- Targeted inhibition of M2 macrophages polarization via a PDC attenuates chronic pancreatitis through the PPARα pathway.iScience · 2026Article
- Peptides in the Diagnosis and Treatment of Pancreatic Cancer and Other Pancreatic Diseases from Basic Research to Clinical Translation.Drug design, development and therapy · 2026Review
- The Ste20 kinase TAOK3 restrains Rac-driven cytoskeletal-mitochondrial coupling to preserve naive CD8Frontiers in immunology · 2026Article
- Extracellular vesicles for macrophage reprogramming: an emerging paradigm in immunomodulatory therapeutics.Journal of biological engineering · 2025Review
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Authors and funding
9 authors.
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Abstract
Background: Chronic pancreatitis (CP) is a fibro-inflammatory syndrome with unclear pathogenesis and futile therapy. CP's microenvironment disrupts the fine-tuned balance of macrophage polarization toward a predominance of the M2-like phenotype associated with fibrosis. S100A9 is mainly expressed in monocytes as a potent regulator of macrophage phenotype and function. Here, we investigated the S100A9-related mechanisms underlying CP pathology induced by macrophages polarization. Methods: Results: In CP progression, S100A9 upregulation induces M2 macrophage polarization to accelerate fibrosis via thousand-and-one amino acid kinase 3 (TAOK3)-c-Jun N-terminal kinase (JNK) signaling pathway, and loss of S100A9 reduces CP injury Conclusions: S100A9 is a significant promoter of M2-like macrophage-induced fibrosis in CP via the TAOK3-JNK signaling pathway. Cobamamide and daptomycin, targeted inhibitors of the S100A9-TAOK3 interaction, may become candidate drugs for CP immunotherapy.
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