ArticleJournal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research2019
Absence of Dipeptidyl Peptidase 3 Increases Oxidative Stress and Causes Bone Loss.
Article in Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed.
- Multiomics profiling of bone in the Dpp3-deficient mice unveils altered protein and lipid composition.Journal of endocrinological investigation · 2026Article
- Dipeptidyl peptidase 3 sets the threshold for immune activation and survival during experimental bacterial infection.Nature communications · 2026Article
- Crosstalk between circulating DPP3 and immune cells in the context of cardio-systemic stress.iScience · 2026Article
- One Enzyme, Many Faces: The Expanding Role of DPP3 in Cardiovascular and Critical Care.Journal of clinical medicine · 2025Review
- Beyond the Genotype: A Multi-Omic Analysis of APOEe4's Role in Alzheimer's Disease.bioRxiv : the preprint server for biology · 2025Article
- Involvement of DPP3 in modulating oncological features and oxidative stress response in esophageal squamous cell carcinoma.Bioscience reports · 2023Article
- Identification of SH2 Domain-Containing Protein 3C as a Novel, Putative Interactor of Dipeptidyl Peptidase 3.International journal of molecular sciences · 2023Article
- Identification of an Additional Metal-Binding Site in Human Dipeptidyl Peptidase III.International journal of molecular sciences · 2023Article
- Effects of Aerobic Dance Exercise and Honey Supplementation Followed by Their Subsequent Cessation on Bone Metabolism Markers and Antioxidant Status in Young Collegiate Females.The Malaysian journal of medical sciences : MJMS · 2023Article
- Article
- The Yin and Yang Effect of the Apelinergic System in Oxidative Stress.International journal of molecular sciences · 2023Review
- Influence of Mutations of Conserved Arginines on Neuropeptide Binding in the DPP III Active Site.Molecules (Basel, Switzerland) · 2023Article
- DPP3 expression promotes cell proliferation and migrationOncology reports · 2023Article
- Association between serum uric acid level and bone mineral density at multiple skeletal sites in middle-aged and elderly men: a cross-sectional study of a healthy population in Taiwan.Archives of osteoporosis · 2022Article
- Dipeptidyl Peptidase 3 Activity as a Promising Biomarker of Bone Fragility in Postmenopausal Women.Molecules (Basel, Switzerland) · 2022Article
- Direct effects of octreotide on osteoblast cell proliferation and function.Journal of endocrinological investigation · 2022Article
- Interdisciplinary Study of the Effects of Dipeptidyl-Peptidase III Cancer Mutations on the KEAP1-NRF2 Signaling Pathway.International journal of molecular sciences · 2022Article
- Label-free multimodal nonlinear optical microscopy reveals features of bone composition in pathophysiological conditions.Frontiers in bioengineering and biotechnology · 2022Article
- DPP3: From biomarker to therapeutic target of cardiovascular diseases.Frontiers in cardiovascular medicine · 2022Review
- Choline Protects the Heart from Doxorubicin-Induced Cardiotoxicity through Vagal Activation and Nrf2/HO-1 Pathway.Oxidative medicine and cellular longevity · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors.
Funding
Abstract
Controlling oxidative stress through the activation of antioxidant pathways is crucial in bone homeostasis, and impairments of the cellular defense systems involved contribute to the pathogenesis of common skeletal diseases. In this work we focused on the dipeptidyl peptidase 3 (DPP3), a poorly investigated ubiquitous zinc-dependent exopeptidase activating the Keap1-Nrf2 antioxidant pathway. We showed Dpp3 expression in bone and, to understand its role in this compartment, we generated a Dpp3 knockout (KO) mouse model and specifically investigated the skeletal phenotype. Adult Dpp3 KO mice showed a mild growth defect, a significant increase in bone marrow cellularity, and bone loss mainly caused by increased osteoclast activity. Overall, in the mouse model, lack of DPP3 resulted in sustained oxidative stress and in alterations of bone microenvironment favoring the osteoclast compared to the osteoblast lineage. Accordingly, in vitro studies revealed that Dpp3 KO osteoclasts had an inherent increased resorptive activity and ROS production, which on the other hand made them prone to apoptosis. Moreover, absence of DPP3 augmented bone loss after estrogen withdrawal in female mice, further supporting its relevance in the framework of bone pathophysiology. Overall, we show a nonredundant role for DPP3 in the maintenance of bone homeostasis and propose that DPP3 might represent a possible new osteoimmunological player and a marker of human bone loss pathology. © 2019 American Society for Bone and Mineral Research.
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.