ArticleCell death discovery2022
SIRT1 restoration enhances chondrocyte autophagy in osteoarthritis through PTEN-mediated EGFR ubiquitination.
Article in Cell death discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 23 citations in OpenAlex.
- Small extracellular vesicles in osteoarthritis: A double‑edged sword regulating inflammation and cartilage homeostasis (Review).International journal of molecular medicine · 2026Review
- DHA-Derived Lipid Mediators Attenuate Osteoarthritis by Resolving Inflammation and Protecting Cartilage in Association with the SIRT1 Signaling Pathway.Marine drugs · 2026Article
- Exploring mitochondrial functions and dysfunctions in chondrocytes: toward the identification of novel therapies for osteoarthritis.Bone research · 2026Review
- Review
- Mechanoepigenetics in musculoskeletal disease.Osteoarthritis and cartilage · 2026Review
- SIRT1 as a Key Regulator in Rheumatic Diseases: Integrating Molecular Insights with Traditional Chinese Medicine Approaches.Journal of inflammation research · 2026Review
- The emerging role of histone acetylation in rheumatic diseases: unraveling mechanisms and therapeutic prospects.Frontiers in immunology · 2026Review
- Sirt1 overexpression inhibits chondrocyte ferroptosis via Ftl deacetylation to suppress the development of osteoarthritis.Journal of bone and mineral metabolism · 2025Article
- Injectable sustainable andrographolide-releasing hydrogel for long-lasting alleviation of osteoarthritis and regulation of chondrocyte autophagy via PRKCA/EGFR.Materials today. Bio · 2025Article
- Article
- Integrated multi-omics and machine learning reveals immune-metabolic signatures in osteoarthritis: from bulk RNA-seq to single-cell resolution.Frontiers in immunology · 2025Article
- PTEN: an emerging target in rheumatoid arthritis?Cell communication and signaling : CCS · 2024Review
- Chondrocyte autophagy mechanism and therapeutic prospects in osteoarthritis.Frontiers in cell and developmental biology · 2024Review
- Estradiol as the Trigger of Sirtuin-1-Dependent Cell Signaling with a Potential Utility in Anti-Aging Therapies.International journal of molecular sciences · 2023Review
- A Gel-Based Proteomic Analysis Reveals Synovial α-Enolase and Fibrinogen β-Chain Dysregulation in Knee Osteoarthritis: A Controlled Trial.Journal of personalized medicine · 2023Article
- Epigenetics as a Therapeutic Target in Osteoarthritis.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Elucidating the role of ubiquitination and deubiquitination in osteoarthritis progression.Frontiers in immunology · 2023Review
- Sirtuins in osteoarthritis: current understanding.Frontiers in immunology · 2023Review
- The sirtuin family in health and disease.Signal transduction and targeted therapy · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pharmacological interventions aimed at activating pathways inducing chondrocyte autophagy or reversing extracellular matrix degradation may be promising approaches for the management of osteoarthritis (OA). Evidence exists suggesting that sirtuin 1 (SIRT1) is involved in the pathogenesis of OA. The present study aimed to explore the regulatory role and downstream mechanisms of SIRT1 in OA. Bioinformatics predictions identified downstream factors phosphatase and tensin homolog (PTEN) and epidermal growth factor receptor (EGFR) in OA. We validated poorly expressed SIRT1 and EGFR and highly expressed PTEN in cartilage tissues of OA patients. OA was induced in vitro by exposing human primary chondrocytes to IL-1β and in vivo by destabilization of the medial meniscus (DMM) in a mouse model. SIRT1 knockdown was found to augment IL-1β-stimulated inflammation and chondrocyte metabolic imbalance. Knockdown of SIRT1 diminished PTEN acetylation and then enhanced PTEN expression. PTEN inactivation decreased EGFR ubiquitination and promoted EGFR expression by destabilizing the EGFR-Cbl complex, which in turn inhibited extracellular matrix degradation in cartilage tissues and activated chondrocyte autophagy. In the DMM mouse model, knockdown of SIRT1 inhibited chondrocyte autophagy, promoted metabolic imbalance, thus accelerating osteoarthritic process. In conclusion, SIRT1 represses the ubiquitination of EGFR by down-regulating PTEN, inhibits extracellular matrix degradation and activates chondrocyte autophagy, thereby performing an OA-alleviating role.
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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.