ArticleArchives of medical science : AMS2023
High glucose promotes apoptosis and autophagy of MC3T3-E1 osteoblasts.
Article in Archives of medical science : AMS, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 20 citations in OpenAlex.
- Bone Healing Around Implants in Normal and Medically Compromised Conditions: Osteoporosis and Diabetes.Advanced healthcare materials · 2026Review
- HOXA7 Impairs Osteogenic Differentiation via p38/JNK Signaling: Implications for Osteoporosis.Journal of musculoskeletal & neuronal interactions · 2026Article
- Molecular mechanisms and preclinical evidence of natural products in diabetic osteoporosis: a review.Frontiers in endocrinology · 2026Review
- Network pharmacology andArchives of medical science : AMS · 2026Article
- Adiposity-lipid-glycemic clusters as potential warning signals of bone mass reduction in Asia's largest urban communities - based bone health assessment via ultrasound.Lipids in health and disease · 2025Article
- New Aspects of the Pathophysiology of Diabetic Bone Fragility - Type 2 Diabetes Mellitus as a Disease of Accelerated Aging.Current osteoporosis reports · 2025Review
- Bidirectional modulation of glycolysis using a multifunctional nanocomposite hydrogel promotes bone fracture healing in type 2 diabetes mellitus.Bioactive materials · 2025Article
- Iron dysregulation, ferroptosis, and oxidative stress in diabetic osteoporosis: Mechanisms, bone metabolism disruption, and therapeutic strategies.World journal of diabetes · 2025Review
- Effects of chloroquine and hydroxychloroquine on bone health (Review).Molecular medicine reports · 2025Review
- Different Forms of Regulated Cell Death in Type-2-Diabetes-Mellitus-Related Osteoporosis: A Focus on Mechanisms and Therapeutic Strategies.International journal of molecular sciences · 2025Review
- Glabridin Alleviates Oxidative Stress-Induced Osteoporosis by Targeting the Akt/NF-ĸB and Akt/GSK-3β Pathways.International journal of molecular sciences · 2025Article
- Research progress of diabetic osteoporosis: a comprehensive review.Frontiers in endocrinology · 2025Review
- The Critical Role of Autophagy in the Pathogenesis of Diabetic Osteoporosis: Mechanisms and Therapeutic Measures.Drug design, development and therapy · 2025Review
- Excessive autophagy of myocardial cells promotes ferroptosis and exacerbates heart failure in the state of myocardial infarction.Archives of medical science : AMS · 2025Article
- Correlation Between Blood Glucose Fluctuations and Osteoporosis in Type 2 Diabetes Mellitus.International journal of endocrinology · 2025Review
- Thioredoxin Interacting Protein Expressed in Osteoblasts Mediates the Anti-Proliferative Effects of High Glucose and Modulates the Expression of Osteocalcin.Journal of bone metabolism · 2024Article
- Acid sphingomyelinase mediates ferroptosis induced by high glucose via autophagic degradation of GPX4 in type 2 diabetic osteoporosis.Molecular medicine (Cambridge, Mass.) · 2023Article
- Circulating MicroRNA-30a, Beclin1 and Their Association with Different Variables in Females with Metabolically Healthy /Unhealthy Obesity.Diabetes, metabolic syndrome and obesity : targets and therapy · 2023Article
- The Potential of Natural Compounds Regulating Autophagy in the Treatment of Osteoporosis.Journal of inflammation research · 2023Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Diabetes and osteoporosis are common metabolic diseases. Abnormal high glucose can lead to the apoptosis of osteoblasts. Autophagy is a highly conserved cellular process that degrades proteins or organelles. In the present study, we comparatively analyzed the effects of high glucose and glucose fluctuation on apoptosis and autophagy of MC3T3-E1 osteoblasts. Material and methods: MC3T3-E1 cells were respectively treated with different concentrations of D-glucose: 5.5 mM for the control group, 25 mM for the high glucose group and 5.5/25 mM for the glucose fluctuation group. Results: High glucose and glucose fluctuation decreased MC3T3-E1 proliferation and activated autophagy. Also, high glucose and glucose fluctuation might induce the production of reactive oxygen species, decline the mitochondrial membrane potential and trigger apoptosis. The differences in the glucose fluctuation treatment group were more significant. Moreover, N-acetylcysteine, an antioxidant reagent, dramatically eliminated the intracellular reactive oxygen species induced by high glucose and glucose fluctuation, and significantly inhibited the autophagy and apoptosis in MC3T3-E1 osteoblasts. Furthermore, treatment with chloroquine, an inhibitor of autophagy, significantly increased the apoptosis of MC3T3-E1 osteoblasts. Conclusions: High glucose, especially high glucose fluctuation, inhibits proliferation and promotes apoptosis and autophagy of MC3T3-E1 osteoblasts. This may occur through inducing oxidative stress and mitochondrial damage in the osteoblasts.
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