ArticleCellular & molecular biology letters2022
Artemisinin relieves osteoarthritis by activating mitochondrial autophagy through reducing TNFSF11 expression and inhibiting PI3K/AKT/mTOR signaling in cartilage.
Article in Cellular & molecular biology letters, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 105 citations in OpenAlex.
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- ROS-responsive injectable hydrogel enables controlled release of human adipose tissue-derived extracellular vesicles for multifaceted osteoarthritis therapy.Journal of nanobiotechnology · 2026Article
- A Combination of Artemisinin, N-acetylcysteine, Resveratrol, and Hesperidin Ameliorates Hippocampal Damage and Pathological Features in an Experimental Model of Alzheimer's Disease.Neurochemical research · 2026Article
- Bioenergetic-active hybrid nanovesicles empower tumor associated macrophages phagocytosis for cancer immunotherapy.Materials today. Bio · 2026Article
- Research progress on cellular senescence in the pathogenesis and treatment of osteoarthritis and temporomandibular joint osteoarthritis.Journal of oral & facial pain and headache · 2026Review
- Modulation of Neuronal Mitochondrial Injury by Gualou Guizhi Decoction in a Mouse Ischemia-Reperfusion Model.Iranian journal of biotechnology · 2026Article
- YTH N6-methyladenosine RNA binding protein 2 mediated mMolecular biomedicine · 2026Article
- IMMT downregulation promotes osteoarthritis development by inducing mitochondrial dysfunction.Journal of orthopaedic surgery and research · 2026Article
- Mechanistic Modulation of Autophagy by Bioactive Natural Products: Implications for Human Aging and Longevity.Nutrients · 2026Review
- Ferroptosis-autophagy crosstalk in bladder cancer: mechanisms and therapeutic implications.Molecular cancer · 2026Review
- Investigating Sex-Linked miRNAs for Potential Osteoarthritis Therapy Biomarkers.International journal of molecular sciences · 2026Article
- Synovial transcriptome analysis reveals ShenTong ZhuYu Tang alleviates osteoarthritis by targeting MMP-9 and immune microenvironment.Journal of orthopaedic surgery and research · 2026Article
- Traditional Chinese medicine-derived monomers delay osteoarthritis progression by regulating mitochondrial homeostasis.Frontiers in cell and developmental biology · 2026Review
- Bu-Fei Formula Ameliorates Inflammation in a Preclinical COPD-Like Model by Targeting Mitochondrial Hyperactivity to Inhibit the NLRP3 Inflammasome.International journal of chronic obstructive pulmonary disease · 2026Article
- New therapeutic target for osteoarthritis: modulating immune-metabolic aberrations and micromilieu remodeling in underlying bone.Frontiers in pharmacology · 2026Review
- The dual role of autophagy in cartilage degradation: from mechanisms to targeted therapeutics.Frontiers in cell and developmental biology · 2026Review
- Astragaloside IV Alleviates Osteoarthritis by Upregulating ETS2: A Bioinformatics and Experimental Study.Journal of inflammation research · 2026Article
- Integrative Multiomics and Network Pharmacology Exploration of Active Components and Mechanisms of Action of Qufu Shengxin Ointment in Treating Chronic Nonhealing Wounds.Mediators of inflammation · 2026Article
1 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 2 institutions in 1 country.
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Abstract
Osteoarthritis (OA) is a widespread chronic degenerative joint disease characterized by the degeneration of articular cartilage or inflamed joints. Our findings indicated that treatment with artemisinin (AT) downregulates the protein levels of MMP3, MMP13, and ADAMTS5, which are cartilage degradation-related proteins in OA, and inhibits the expression of inflammatory factors in interleukin-1β (IL-1β)-stimulated chondrocytes. However, the mechanism of the role of AT in OA remains unclear. Here, we performed gene sequencing and bioinformatics analysis in control, OA, and OA + AT groups to demonstrate that several mRNA candidates were enriched in the PI3K/AKT/mTOR signaling pathway, and TNFSF11 was significantly downregulated after AT treatment. TNFSF11 was downregulated in the OA + AT group, whereas it was upregulated in rat OA tissues and OA chondrocytes. Therefore, we confirmed that TNFSF11 was the target gene of AT. In addition, our study revealed that AT relieved cartilage degradation and defection by activating mitochondrial autophagy via inhibiting the PI3K/AKT/mTOR signaling pathway in IL-1β-induced chondrocytes. Furthermore, an OA model was established in rats with medial meniscus destabilization. Injecting AT into the knee joints of OA rat alleviated surgical resection-induced cartilage destruction. Thus, these findings revealed that AT relieves OA by activating mitochondrial autophagy by reducing TNFSF11 expression and inhibiting PI3K/AKT/mTOR signaling.
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