ArticleCell death & disease2018
RAGE-dependent mitochondria pathway: a novel target of silibinin against apoptosis of osteoblastic cells induced by advanced glycation end products.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.
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Who cites it
53 citing papers in PubMed, 1 synthesis or guideline pooled it, 87 citations in OpenAlex.
- Silibinin as a major component of milk thistle seed provides promising influences against diabetes and its complications: a systematic review.Naunyn-Schmiedeberg's archives of pharmacology · 2024Pooled it
- Glucose metabolism in osteoporosis: A potential therapeutic target (Review).International journal of molecular medicine · 2026Review
- Cardiac metabolic remodeling drives dicarbonyl stress-induced mitochondrial dysfunction in experimental heart failure with preserved ejection fraction.American journal of physiology. Heart and circulatory physiology · 2026Article
- Does the definition of human ultra-processed foods apply to dog and cat foods? A review of pet food processing techniques, their impact on health, and a call for pet food processing classification.Frontiers in veterinary science · 2026Article
- Sea buckthorn seed oil triggers mitochondrial dysfunction and apoptosis inFrontiers in microbiology · 2026Article
- Mitigating mitochondrial dysfunction: a novel strategy for Chinese botanical drugs against osteoporosis.Frontiers in pharmacology · 2026Review
- Decoding the Bone-Eye Axis: Machine Learning for Age-Related Macular Degeneration Risk Prediction.Cyborg and bionic systems (Washington, D.C.) · 2026Article
- Amyloid-beta glycation induces neuronal mitochondrial dysfunction and Alzheimer's pathogenesis via VDAC1-dependent mtDNA efflux.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The hidden driver of osteoporosis: mitochondria-dominated inflammation.Cell communication and signaling : CCS · 2025Review
- Diabetic bone fragility through advanced glycation end product-collagen axis: Mechanisms and therapy of sodium glucose cotransporter 2 inhibitors.World journal of diabetes · 2025Review
- Role of Advanced Glycation End Products and Mitohormesis in Cancer Development and Progression.Antioxidants (Basel, Switzerland) · 2025Review
- Aqueous extract ofBiochemistry and biophysics reports · 2025Article
- An emerging role of mitochondrial quality control in bone metabolism: from molecular mechanisms to targeted therapeutic interventions.Cellular and molecular life sciences : CMLS · 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
- Elevated levels of S100A8 and S100A9 exacerbate muscle mitochondrial fragmentation in sepsis-induced muscle atrophy.Communications biology · 2025Article
- The Potential Mechanism of D-Amino Acids - Mitochondria Axis in the Progression of Diabetic Kidney Disease.Kidney international reports · 2025Review
- Mitochondria: a key regulator of programmed cell death in OP.Frontiers in endocrinology · 2025Review
- Interruption of mitochondrial symbiosis is associated with the development of osteoporosis.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
- TNF receptor-associated factors: promising targets of natural products for the treatment of osteoporosis.Frontiers in physiology · 2025Review
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Advanced glycation end products (AGEs) can stimulate osteoblast apoptosis and have a critical role in the pathophysiology of diabetic osteoporosis. Mitochondrial abnormalities are closely related to osteoblast dysfunction. However, it remains unclear whether mitochondrial abnormalities are involved in AGE-induced osteoblastic cell apoptosis. Silibinin, a major flavonolignan compound of silimarin, has strong antioxidant and mitochondria-protective properties. In the present study, we explored the possible mitochondrial mechanisms underlying AGE-induced apoptosis of osteoblastic cells and the effect of silibinin on osteoblastic cell apoptosis. We demonstrated that mitochondrial abnormalities largely contributed to AGE-induced apoptosis of osteoblastic cells, as evidenced by enhanced mitochondrial oxidative stress, conspicuous reduction in mitochondrial membrane potential and adenosine triphosphate production, abnormal mitochondrial morphology, and altered mitochondrial dynamics. These AGE-induced mitochondrial abnormalities were mainly mediated by the receptor of AGEs (RAGE). In addition, we found that silibinin directly downregulated the expression of RAGE and modulated RAGE-mediated mitochondrial pathways, thereby preventing AGE-induced apoptosis of osteoblastic cells. This study not only provides a new insight into the mitochondrial mechanisms underlying AGE-induced osteoblastic cell apoptosis, but also lays a foundation for the clinical use of silibinin for the prevention or treatment of diabetic osteoporosis.
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