ArticleInflammation2023
The Effect of JAK Inhibitor Tofacitinib on Chondrocyte Autophagy.
Article in Inflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- In vitro evaluation of hydroxyapatite, β-tricalcium phosphate, graphene oxide and zinc oxide for osteochondral regeneration under inflammatory conditions.Molecular and cellular biochemistry · 2026Article
- Smart Nanodelivery Systems for Immunometabolic Modulation in Osteoarthritis.Exploration (Beijing, China) · 2026Review
- Inflammaging and osteoarthritis - therapeutic opportunities.Frontiers in immunology · 2026Review
- Targeting p21-Positive Senescent Chondrocytes via IL-6R/JAK2 Inhibition to Alleviate Osteoarthritis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Key Role of STAT3 in Osteoarthritis: From Pathogenic Mechanisms to Targeted Therapy.International journal of nanomedicine · 2025Review
- Epigenetic Regulation of Autophagy in Bone Metabolism.Function (Oxford, England) · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Osteoarthritis (OA) is a multifactorial disease of the whole joint that has a complex pathogenesis. There is currently no cure for OA. Tofacitinib is a broad JAK inhibitor that can have an anti-inflammatory effect. The objective of this study was to investigate the effect of tofacitinib on the cartilage extracellular matrix in OA and determine whether tofacitinib exerts a protective effect by inhibiting the JAK1/STAT3 signaling pathway and upregulating autophagy in chondrocytes. We investigated the expression profile of OA in vitro by exposing SW1353 cells to interleukin-1β (IL-1β), and induced OA in vivo using the modified Hulth method in rats. We found that IL-1β promoted the expression of OA-related matrix metalloproteinases (MMP3 and MMP13), reduced the expression of collagen II, reduced the expression of beclin1 and LC3-II/I, and promoted the accumulation of p62 in SW1353 cells. Tofacitinib attenuated IL-1β-stimulated changes in MMPs and collagen II and restored autophagy. In IL-1β-stimulated SW1353 cells, the JAK1/STAT3 signaling pathway was activated. Tofacitinib inhibited the IL-1β-stimulated expression of p-JAK1 and p-STAT3 and prevented translocation of p-STAT3 to the nucleus. In the rat model of OA, tofacitinib reduced articular cartilage degeneration by delaying cartilage extracellular matrix degradation and increasing chondrocyte autophagy. Our study demonstrates that chondrocyte autophagy was impaired in experimental models of OA. Tofacitinib reduced the inflammatory response and restored the damaged autophagic flux in OA.
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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 OpenQuestion graph.