ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Dipeptidyl Peptidase 4 (DPP4) Exacerbates Osteoarthritis Progression in an Enzyme-Independent Manner.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
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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.
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Who cites it
7 citing papers in PubMed.
- Adipose-derived mesenchymal stem cell injection into the KI10 acupoint mitigates cartilage damage in KOA rats through PGE2-mediated α7nAChR/NF-κB pathway.Animal models and experimental medicine · 2026Article
- Targeting the SARM1-cADPR-CaArthritis research & therapy · 2026Article
- Targeting the mitochondrial metabolite-dynamics-MDVs-MitoEVs axis: a new frontier in osteoarthritis management.Journal of translational medicine · 2026Review
- Immunoinflammation and post-translational modifications in the aging process.Journal of translational medicine · 2025Review
- A Molecular Chemical Perspective: Mitochondrial Dynamics Is Not a Bystander of Cartilage Diseases.ACS pharmacology & translational science · 2025Review
- Dipeptidyl Peptidase 4 (DPP4) Exacerbates Osteoarthritis Progression in an Enzyme-Independent Manner.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The potential of mitochondrial transfer as the modifying therapy for osteoarthritis.Frontiers in cell and developmental biology · 2025Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Chondrocyte senescence is a key driver of osteoarthritis (OA). Mitochondrial dysfunction and oxidative stress can induce chondrocyte senescence. However, the specific mechanisms by which senescence contributes to OA progression are not fully understood. Here, it is attested that Dipeptidyl peptidase 4 (DPP4) is significantly upregulated in osteoarthritic chondrocytes in both humans and mice. DPP4 promotes oxidative stress and cellular senescence in chondrocytes through excessive mitochondrial fission in an enzyme-independent manner. Intra-articular injection of adeno-associated virus 2 to upregulate DPP4 in chondrocytes promotes post-traumatic and aging-induced OA in mice in an enzyme-independent manner. Mechanistically, DPP4 competitively binds to Myosin heavy chain 9 (MYH9), interfering with its E3 ubiquitin ligase Carboxyl terminus of Hsc70-interacting protein (CHIP), and thereby upregulates MYH9 expression. Finally, a small molecule, 4,5-Dicaffeoylquinic acid is identified, which disrupts the interaction between DPP4 and MYH9, thereby ameliorating post-traumatic and aging-induced OA in mice caused by DPP4 upregulation. The study indicates that the non-enzymatic activity of DPP4 is a promising target for OA treatment.
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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 Socratic graph.