ArticleFrontiers in cellular and infection microbiology2019
Dpep2 Emerging as a Modulator of Macrophage Inflammation Confers Protection Against CVB3-Induced Viral Myocarditis.
Article in Frontiers in cellular and infection microbiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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26 citing papers in PubMed, 36 citations in OpenAlex.
- Intracellular Staphylococcus aureus triggers isolate-specific host transcriptional responses alongside TNF-R1 regulated cell fate decisions.Cell communication and signaling : CCS · 2026Article
- Integrative exome sequencing and multi-omics analysis elucidates the regulatory role of rare variants in metabolic syndrome.Functional & integrative genomics · 2026Article
- Targeting the Myocardial Microenvironment: Novel Antiviral Strategies and Therapeutic Perspectives for Coxsackievirus B-Induced Myocarditis.Journal of the American Heart Association · 2026Review
- DPEP2 suppresses hyperinflammation via metabolic reprogramming of macrophages in sepsis.Nature communications · 2026Article
- 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
- The Trim32-DPEP2 axis is an inflammatory switch in macrophages during intestinal inflammation.Cell death and differentiation · 2025Article
- Host-virus interactions during infection with a wild-type ILTV strain or a glycoprotein G deletion mutant ILTV vaccine strain in anMicrobiology spectrum · 2025Article
- Article
- Exploring the Potential Regulatory Mechanisms of Mitophagy in Ischemic Cardiomyopathy.International journal of general medicine · 2025Article
- Insight into dipeptidase 1: structure, function, and mechanism in gastrointestinal cancer diseases.Translational cancer research · 2024Review
- A High-Quality Blue Whale Genome, Segmental Duplications, and Historical Demography.Molecular biology and evolution · 2024Article
- M2 macrophage exosome-derived lncRNA AK083884 protects mice from CVB3-induced viral myocarditis through regulating PKM2/HIF-1α axis mediated metabolic reprogramming of macrophages.Redox biology · 2024Article
- Dipeptidase‑2 is a prognostic marker in lung adenocarcinoma that is correlated with its sensitivity to cisplatin.Oncology reports · 2023Article
- Integrated Single-Cell and Transcriptome Sequencing Analyses Identify Dipeptidase 2 as an Immune-Associated Prognostic Biomarker for Lung Adenocarcinoma.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Role of Coxsackievirus B3-Induced Immune Responses in the Transition from Myocarditis to Dilated Cardiomyopathy and Heart Failure.International journal of molecular sciences · 2023Review
- An immune indicator based on BTK and DPEP2 identifies hot and cold tumors and clinical treatment outcomes in lung adenocarcinoma.Scientific reports · 2023Article
- Plasma protein changes reflect colorectal cancer development and associated inflammation.Frontiers in oncology · 2023Article
- Exploring the biological function of immune cell-related genes in human immunodeficiency virus (HIV)-1 infection based on weighted gene co-expression network analysis (WGCNA).BMC medical genomics · 2022Article
- The aryl hydrocarbon receptor instructs the immunomodulatory profile of a subset of Clec4a4Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Identification of shared and disease-specific host gene-microbiome associations across human diseases using multi-omic integration.Nature microbiology · 2022Article
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3 authors at 1 institution in 1 country.
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Abstract
Overwhelming cardiac inflammation has been reported to be the pathogenic mechanism of Coxsackievirus B3 (CVB3)-induced viral myocarditis (VMC), while the detailed molecular mechanisms remain unknown. Membrane-bound dipeptidases (MBD, also known as Dpep) have been shown to be involved in inflammatory diseases. However, the clear and direct evidence of their impacts on inflammation is still lacking. In this study, our results revealed that Dpep2 expression was remarkably increased during CVB3 infection, and primarily produced by the cardiac tissue-infiltrating macrophages instead of constitutive cardiomyocytes. Macrophages have been reported to play an important pathological role in driving VMC. Interestingly, macrophage-specific Dpep2 deletion robustly aggravated CVB3-induced cardiac inflammation, evidenced by augmented expression of TNF-α, IL-6, and MCP-1 in heart tissue. In addition, Dpep2-deficient bone-marrow derived macrophages (BMDMs) generated more TNF-α, IL-6, and MCP-1 after CVB3 stimulation compared with the control BMDMs. Moreover, this suppressive effect of Dpep2 on macrophages relied on its repression on NF-κB signaling pathway, but not on its conventional hydrolysate LTE4. Taken together, this study revealed that Dpep2 could protect against CVB3-induced VMC by acting as a suppressor of macrophage inflammation. Better understanding how macrophage Dpep2 dampened the cardiac inflammation would provide us with insights for the efficient control of CVB3-induced VMC.
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