ArticleCell death & disease2021
High glucose suppresses autophagy through the AMPK pathway while it induces autophagy via oxidative stress in chondrocytes.
Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.
- Effectiveness of metformin in the management of osteoarthritis in patients with type 2 diabetes.Clinical rheumatology · 2026 · on this mapPooled it
- Gut‑liver‑kidney axis: A systems biology framework for understanding and treating chronic kidney disease (Review).International journal of molecular medicine · 2026Review
- Autophagy and metabolic homeostasis: Exploration in obesity‑related metabolic diseases (Review).International journal of molecular medicine · 2026Review
- The Interaction Between Mitophagy Dysregulation and the Diabetic Bladder Microenvironment.Journal of diabetes · 2026Review
- Structural and Molecular Effects of Dextrose on Cartilage: A Scoping Review.Current rheumatology reviews · 2026Article
- Potential crosstalk between ferroptosis and immunosenescence in osteoarthritis: evidence integration and translational insights from the osteoimmune microenvironment.Frontiers in immunology · 2026Review
- Cartilage Redox Balance Is Influenced by Substrate Availability.Cartilage · 2025Article
- Lipoic acid-plumbagin conjugate protects pancreatic beta cells against high glucose-induced toxicity.Scientific reports · 2025Article
- Exploring the Multifactorial Regulation of PIEZO1 in Chondrocytes: Mechanisms and Implications.International journal of medical sciences · 2025Review
- Gossypol Acetic Acid Alleviates the Ferroptosis of Chondrocytes in Osteoarthritis by Inhibiting GPX4 Methylation.Current medicinal chemistry · 2025Article
- AMPK signaling in osteoarthritis: from mechanisms to targeted therapeutics.Frontiers in pharmacology · 2025Review
- High glucose condition aggravates inflammatory response induced by Porphyromonas gingivalis in THP-1 macrophages via autophagy inhibition.BMC immunology · 2024Article
- HDAC1 Promotes Mitochondrial Pathway Apoptosis and Inhibits the Endoplasmic Reticulum Stress Response in High Glucose-Treated Schwann Cells via Decreased U4 Spliceosomal RNA.Neurochemical research · 2024Article
- Poricoic acid a ameliorates high glucose-induced podocyte injury by regulating the AMPKα/FUNDC1 pathway.Molecular biology reports · 2024Article
- Cell culture-derived extracellular vesicles: Considerations for reporting cell culturing parameters.Journal of extracellular biology · 2023Article
- The Beneficial and Adverse Effects of Autophagic Response to Caloric Restriction and Fasting.Advances in nutrition (Bethesda, Md.) · 2023Review
- Pyruvate Dehydrogenase Kinase 1 inhibition mediated oxidative phosphorylation enhancement in cartilage promotes osteoarthritis progression.BMC musculoskeletal disorders · 2023Article
- Hyperglycemia Aggravates Periodontitis via Autophagy Impairment and ROS-Inflammasome-Mediated Macrophage Pyroptosis.International journal of molecular sciences · 2023Article
- HIF-1α upregulation exerts the antagonistic effect against angiogenesis inhibition in manganese deficiency-induced tibial dyschondroplasia of broiler chicks.Veterinary research communications · 2022Article
- Review
Corrections and comments
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetes (DB) is a risk factor for osteoarthritis progression. High glucose (HG) is one of the key pathological features of DB and has been demonstrated to induce apoptosis and senescence in chondrocytes. Autophagy is an endogenous mechanism that can protect cells against apoptosis and senescence. The effects of HG on autophagy in cells including chondrocytes have been studied; however, the results have been inconsistent. The current study aimed to elucidate the underlying mechanisms, which could be associated with the contrasting outcomes. The present study revealed that HG can induce apoptosis and senescence in chondrocytes, in addition to regulating autophagy dynamically. The present study demonstrated that HG can cause oxidative stress in chondrocytes and suppress the AMPK pathway in a dose-dependent manner. Elimination of oxidative stress by Acetylcysteine, also called N-acetyl cysteine (NAC), downregulated autophagy and alleviated HG-stimulated apoptosis and senescence, while activation of the AMPK signaling pathway by AICAR not only upregulated autophagy but also alleviated HG-stimulated apoptosis and senescence. A combined treatment of NAC and AICAR was superior to treatment with either NAC or AICAR. The study has demonstrated that HG can suppress autophagy through the AMPK pathway and induce autophagy via oxidative stress in chondrocytes.
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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.