ArticleCell death & disease2017
Trehalose ameliorates oxidative stress-mediated mitochondrial dysfunction and ER stress via selective autophagy stimulation and autophagic flux restoration in osteoarthritis development.
Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 132 papers, 1 of them a synthesis that pooled it.
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Who cites it
132 citing papers in PubMed, 1 synthesis or guideline pooled it, 263 citations in OpenAlex.
- Multi-target synergistic mechanisms of flavonoid compounds from traditional Chinese medicine in non-alcoholic fatty liver disease: insights for human and veterinary medicine.Frontiers in veterinary science · 2026Pooled it
- SIRT3-mediated DRP1 acetylation changes are associated with the restoration of mitochondrial function and alleviation of anterior cruciate ligament injury-induced osteoarthritis.Journal of molecular histology · 2026Article
- Repetitive Compressive Loading Downregulates the Expression of Autophagy-Related Factors, Autophagy Capacity and Cellular Activity in Human Osteoarthritic Chondrocytes.International journal of molecular sciences · 2026Article
- High glucose impairs autophagy and mitochondrial homeostasis in human dental pulp cells.Scientific reports · 2026Article
- Calcium oxalate crystals exacerbate the damage and inflammation of renal tubular epithelial cells by blocking autophagic flux.Urolithiasis · 2026Article
- Trehalose as an anti-inflammatory agent: insights into molecular mechanisms and therapeutic applications.Inflammopharmacology · 2026Review
- Osteoarthritis: molecular pathogenesis and potential therapeutic options.Signal transduction and targeted therapy · 2026Review
- Repurposing metformin for treating osteoarthritis via leveraging Nrf2 signaling.Scientific reports · 2026Article
- Advances in Research on Autophagy in Steroid-Induced Osteonecrosis of the Femoral Head: Dual Regulation of Its Beneficial and Detrimental Effects.Drug design, development and therapy · 2026Review
- Repeated Exposure to Lidocaine Induces Alzheimer's‐Like Cognitive Impairment and Neuropathology in Aged Mice Through BDNF‐Regulated Autophagy.Journal of cellular and molecular medicine · 2025Article
- Mammalian Sterile 20-Like Kinase 2 Knockdown Alleviates Neuropathic Pain in Rats by Mitochondrial Protection.Molecular neurobiology · 2025Article
- Curcumin controls the senescence of adipose-derived mesenchymal stem cells via the FoxO3/autophagy signaling pathway to enhance joint homeostasis for osteoarthritis therapy.Stem cell research & therapy · 2025Article
- Article
- MiR-ON-CRISPR: a microRNA-activated CRISPR-dCas9 system for precise gene therapy in living cells and mouse models of sepsis.Nucleic acids research · 2025Article
- The impact of mitochondrial dysfunction on osteoarthritis cartilage: current insights and emerging mitochondria-targeted therapies.Bone research · 2025Review
- The Tacrine-Induced Endoplasmic Reticulum Stress in AChE-Expressed Cells Leads to Improper Assembly and Transport of the Oligomeric Enzyme: Reversal by Trehalose.Journal of neurochemistry · 2025Article
- Asperosaponin VI mitigates mitochondrial dysfunction and chondrocyte apoptosis in osteoarthritis by modulating the AMPK-SIRT3 pathway.Cell biology and toxicology · 2025Article
- The dual role of PGAM5 in inflammation.Experimental & molecular medicine · 2025Review
- The Pathophysiological Role of Mitochondrial Oxidative Stress in Rheumatic Diseases.Journal of inflammation research · 2025Review
- Dietary phenolics and exercise complementation to delay aging at its source: a comprehensive review highlighting mitochondrial function.Frontiers in aging · 2025Review
72 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oxidative stress-related apoptosis and autophagy play crucial roles in the development of osteoarthritis (OA), a progressive cartilage degenerative disease with multifactorial etiologies. Here, we determined autophagic flux changes and apoptosis in human OA and tert-Butyl hydroperoxide (TBHP)-treated chondrocytes. In addition, we explored the potential protective effects of trehalose, a novel Mammalian Target of Rapamycin (mTOR)-independent autophagic inducer, in TBHP-treated mouse chondrocytes and a destabilized medial meniscus (DMM) mouse OA model. We found aberrant p62 accumulation and increased apoptosis in human OA cartilage and chondrocytes. Consistently, p62 and cleaved caspase-3 levels increased in mouse chondrocytes under oxidative stress. Furthermore, trehalose restored oxidative stress-induced autophagic flux disruption and targeted autophagy selectively by activating BCL2 interacting protein 3 (BNIP3) and Phosphoglycerate mutase family member 5 (PGAM5). Trehalose could ameliorate oxidative stress-mediated mitochondrial membrane potential collapse, ATP level decrease, dynamin-related protein 1 (drp-1) translocation into the mitochondria, and the upregulation of proteins involved in mitochondria and endoplasmic reticulum (ER) stress-related apoptosis pathway. In addition, trehalose suppressed the cleavage of caspase 3 and poly(ADP-ribose) polymerase (PARP) and prevented DNA damage under oxidative stress. However, the anti-apoptotic effects of trehalose in TBHP-treated chondrocytes were partially abolished by autophagic flux inhibitor chloroquine and BNIP3- siRNA. The protective effect of trehalose was also found in mouse OA model. Taken together, these results indicate that trehalose has anti-apoptotic effects through the suppression of oxidative stress-induced mitochondrial injury and ER stress which is dependent on the promotion of autophagic flux and the induction of selective autophagy. Thus, trehalose is a promising therapeutic agent for OA.
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