ArticleFrontiers in immunology2025
Identification of Grb2 protein as a potential mediator of macrophage activation in acute pancreatitis based on bioinformatics and experimental verification.
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 5 papers.
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Who cites it
5 citing papers in PubMed.
- NLRP3 Regulation in Neonatal Hypoxic-Ischemic Encephalopathy-Focus on Microglial Activation.International journal of molecular sciences · 2026Article
- Adaptor proteins regulating tumor-associated macrophage polarization during cancer progression.Oncoscience · 2026Review
- Spatiotemporal Heterogeneity of Macrophages in Acute Pancreatitis: From Inflammatory Initiators to Repair Coordinators and Targeted Therapeutics.Mediators of inflammation · 2026Review
- Celastrol Mitigates Acute Pancreatitis Associated Inflammation by Modulating the IL-34/CSF-1R Axis and Suppressing NF-κB/ERK Signaling.Journal of inflammation research · 2026Article
- CD44 and CLDN3 as immune-metabolic regulators in acute pancreatitis: a multi-modal transcriptomics study and experimental validation.Frontiers in immunology · 2025Article
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12 authors.
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Abstract
Introduction: Macrophage activation is closely associated with Acute pancreatitis (AP). We screened and found that Growth factor receptor bound protein 2 (Grb2) is highly expressed in macrophages during AP. However, the relationship between Grb2 and AP is still poorly understood. In this study, we explored the role of Grb2 in AP. Methods: We screened for gene affecting macrophage activation in AP by combining transcriptomics with Single-cell RNA-sequence analysis. Next, the expression of Grb2 in M1/M2 macrophage activation was detected by Single-cell RNA-sequence analysis and western blot. Furthermore, the effect of Grb2 on M1/M2 macrophage activation was detected by flow cytometry. The severity of AP was assessed by histological analysis, serum amylase, serum lipase and serum inflammatory factors Results: Grb2 is mainly expressed in macrophages of pancreas in AP and up-regulated in M1 macrophage activation. Inhibiting Grb2 could alleviate AP by preventing M1 macrophage activation through down-regulating Nlrp3 and NF-κB. Discussion: Inhibition of Grb2 can effectively prevent M1 macrophage activation and alleviate AP. Grb2 may potentially be an effective target of macrophage activation for the treatment of AP.
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