ArticleCell death and differentiation2025
The Trim32-DPEP2 axis is an inflammatory switch in macrophages during intestinal inflammation.
Article in Cell death and differentiation, 2025. 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.
- Intracellular Staphylococcus aureus triggers isolate-specific host transcriptional responses alongside TNF-R1 regulated cell fate decisions.Cell communication and signaling : CCS · 2026Article
- The Target ALS Global Natural History Study: Cross-platform proteomics to accelerate biofluid biomarker and drug target discovery in amyotrophic lateral sclerosis.medRxiv : the preprint server for health sciences · 2026Article
- Fluorescence-Guided Spatial Mapping of p21-Expressing Senescent Cells in Aged Liver at Single-Cell Resolution.Biomolecules · 2026Article
- DPEP2 suppresses hyperinflammation via metabolic reprogramming of macrophages in sepsis.Nature communications · 2026Article
- Roles and Mechanisms of TRIM Family Proteins in Inflammation in the Brain and Beyond.International journal of molecular sciences · 2026Review
- The role of TRIM proteins in the pathogenesis of mycobacterium tuberculosis.Biology direct · 2025Review
- DPEP2 suppresses metastasis via NF-κB-mediated epithelial-mesenchymal transition and M2 polarization in p53-loss non-small cell lung cancer.Cancer cell international · 2025Article
- Article
- HMGB1 Derived from the Pyroptotic Microenvironment Promotes Macrophage Extracellular Traps in Hirschsprung-Associated Enterocolitis.Advanced biology · 2025Article
- Article
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11 authors.
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Abstract
The mechanisms via which inflammatory macrophages mediate intestinal inflammation are not completely understood. Herein, using merged analysis of RNA sequencing and mass spectrometry-based quantitative proteomics, we detected differences between proteomic and transcriptomic data in activated macrophages. Dipeptidase-2 (DPEP2), a member of the DPEP family, was highly expressed and then downregulated sharply at the protein level but not at the mRNA level in macrophages in response to inflammatory stimulation. Suppression of DPEP2 not only enhanced macrophage-mediated intestinal inflammation in vivo but also promoted the transduction of inflammatory pathways in macrophages in vitro. Mechanistically, overexpressed DPEP2 inhibited the transduction of inflammatory signals by resisting MAK3K7 in inactivated macrophages, whereas DPEP2 degradation by activated Trim32 resulted in strong activation of NF-κB and p38 MAPK signaling via the release of MAK3K7 in proinflammatory macrophages during the development of intestinal inflammation. The Trim32-DPEP2 axis accumulates the potential energy of inflammation in macrophages. These results identify DPEP2 as a key regulator of macrophage-mediated intestinal inflammation. Thus, the Trim32-DPEP2 axis may be a potential therapeutic target for the treatment of intestinal inflammation.
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