ArticleAmerican journal of translational research2019
Sitagliptin ameliorates advanced glycation end-product (AGE)-induced degradation of extracellular matrix in human primary chondrocytes.
Article in American journal of translational research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Inflammatory mechanisms underlying metabolic syndrome-associated and potential treatments.Osteoarthritis and cartilage open · 2025Article
- The role of AGEs in pathogenesis of cartilage destruction in osteoarthritis.Bone & joint research · 2022Article
- Emerging Role of Dipeptidyl Peptidase-4 in Autoimmune Disease.Frontiers in immunology · 2022 · on this mapReview
- Antioxidative Potentials of Incretin-Based Medications: A Review of Molecular Mechanisms.Oxidative medicine and cellular longevity · 2021Review
- Dexmedetomidine exerts dual effects on human annulus fibrosus chondrocytes depending on the oxidative stress status.Bioscience reports · 2019Article
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Accumulation of advanced glycation end-products (AGEs) increases inflammation and triggers processes involved in the pathogenesis of osteoarthritis (OA). As a major debilitating age-related disease, it is imperative that novel therapies for OA be sought. In the present study, we investigated the effects of the selective dipeptidyl peptidase IV (DPP-4) inhibitor sitagliptin in human primary chondrocytes exposed to insult by AGEs to elucidate the potential role of sitagliptin in the treatment of OA. Our findings show that inhibition of DPP-4 by sitagliptin could reduce oxidative stress, increase cell viability and prevent degradation of type II collagen and aggrecan by matrix metalloproteinases (MMPs) and a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS) induced by AGEs in human primary chondrocytes. Mechanistically, we found that sitagliptin inhibited AGEs-induced nuclear translocation of p65 protein and drastically decreased the luciferase activity of NF-κB. These findings indicate that sitagliptin may have potential as a novel therapeutic option for the treatment and prevention of OA.
Indexed as
Identifiers
31217853PMC6556674W2980813053What 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.