ArticleInflammation2016
The Dipeptidyl Peptidases 4, 8, and 9 in Mouse Monocytes and Macrophages: DPP8/9 Inhibition Attenuates M1 Macrophage Activation in Mice.
Article in Inflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 39 citations in OpenAlex.
- Identification and functional characterization of regulatory variants in DPP9 associated with COVID-19 severity.Genome medicine · 2026Article
- DPP-4 Inhibitors in Female Cancers: Opportunities for Drug Repurposing.Current issues in molecular biology · 2026Review
- A fluorescent sensor for real-time monitoring of DPP8/9 reveals crucial roles in immunity and cancer.Life science alliance · 2025Article
- Targeting dipeptidyl peptidase-8/9 to combat inflammation-induced osteoclastogenesis in RAW264.7 macrophages and analysis of anti-osteoclastogenesis potential of chrysin.Iranian journal of basic medical sciences · 2025Article
- Pinocembrin activation of DPP9 inhibits NLRP1 inflammasome activation to alleviate cerebral ischemia/reperfusion-induced lung and intestinal injury.Immunologic research · 2024Article
- CD26 Deficiency Controls Macrophage Polarization Markers and Signal Transducers during Colitis Development and Resolution.International journal of molecular sciences · 2022Article
- New insights into the role of dipeptidyl peptidase 8 and dipeptidyl peptidase 9 and their inhibitors.Frontiers in pharmacology · 2022Review
- Article
- Dipeptidyl peptidase 4 inhibitors: Applications in innate immunity?Biochemical pharmacology · 2021Review
- Alpha-1 Antitrypsin-Expressing Mesenchymal Stromal Cells Confer a Long-Term Survival Benefit in a Mouse Model of Lethal GvHD.Molecular therapy : the journal of the American Society of Gene Therapy · 2019Article
- Immune regeneration in irradiated mice is not impaired by the absence of DPP9 enzymatic activity.Scientific reports · 2019Article
- DPP8/DPP9 inhibition elicits canonical Nlrp1b inflammasome hallmarks in murine macrophages.Life science alliance · 2019Article
- Structures and mechanism of dipeptidyl peptidases 8 and 9, important players in cellular homeostasis and cancer.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Contribution of upregulated dipeptidyl peptidase 9 (DPP9) in promoting tumoregenicity, metastasis and the prediction of poor prognosis in non-small cell lung cancer (NSCLC).International journal of cancer · 2017Article
- The expression of proline-specific enzymes in the human lung.Annals of translational medicine · 2017Review
- Article
- DPP8 and DPP9 inhibition induces pro-caspase-1-dependent monocyte and macrophage pyroptosis.Nature chemical biology · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atherosclerosis remains the leading cause of death in Western countries. Dipeptidyl peptidase (DPP) 4 has emerged as a novel target for the prevention and treatment of atherosclerosis. Family members DPP8 and 9 are abundantly present in macrophage-rich regions of atherosclerotic plaques, and DPP9 inhibition attenuates activation of human M1 macrophages in vitro. Studying this family in a mouse model for atherosclerosis would greatly advance our knowledge regarding their potential as therapeutic targets. We found that DPP4 is downregulated during mouse monocyte-to-macrophage differentiation. DPP8 and 9 expression seems relatively low in mouse monocytes and macrophages. Viability of primary mouse macrophages is unaffected by DPP4 or DPP8/9 inhibition. Importantly, DPP8/9 inhibition attenuates macrophage activation as IL-6 secretion is significantly decreased. Mouse macrophages respond similarly to DPP inhibition, compared to human macrophages. This shows that the mouse could become a valid model species for the study of DPPs as therapeutic targets in atherosclerosis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.