ArticleRedox biology2021
Sirt3-mediated mitophagy regulates AGEs-induced BMSCs senescence and senile osteoporosis.
Article in Redox biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 161 papers, 6 of them syntheses that pooled it.
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Who cites it
161 citing papers in PubMed, 6 syntheses or guidelines pooled it, 275 citations in OpenAlex.
- From mechanisms to therapeutics: a narrative review on pyroptosis and autophagy in osteoporosis.Annals of medicine · 2025Pooled it
- Rejuvenation of Bone Marrow Mesenchymal Stem Cells: Mechanisms and Their Application in Senile Osteoporosis Treatment.Biomolecules · 2025Pooled it
- Efficacy and safety of acupuncture as an adjuvant therapy for osteoporosis: a systematic review and meta-analysis of randomized controlled trials.Frontiers in endocrinology · 2025Pooled it
- Mitochondria: a breakthrough in combating rheumatoid arthritis.Frontiers in medicine · 2024Pooled it
- Application of rhBMP in spinal fusion surgery: any correlation of cancer incidence? A systematic review and meta-analysis.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2023Pooled it
- Effects of advanced glycation end products (AGEs) on the differentiation potential of primary stem cells: a systematic review.Stem cell research & therapy · 2023Pooled it
- A dual-targeting mRNA lipid nanoparticle restores ABCA1-dependent cholesterol homeostasis to promote repair of age-related bone defects.Bioactive materials · 2027Article
- Mitochondria-transplanted macrophages: a novel strategy targeting mitochondrial dysfunction to enhance myocardial repair after myocardial infarction.MedScience · 2026Article
- SIRT3-dependent mitochondrial redox homeostasis protects against age-related tendon degeneration.Bone & joint research · 2026Article
- Naringenin ameliorates postmenopausal osteoporosis by inhibiting BMSC oxidative stress via the PI3K/AKT/NRF2 pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Bone organoids and mitochondrial reprogramming.Journal of orthopaedic translation · 2026Review
- Review
- GLP-1 regulates osteo-adipogenic fate of BMSCs via HIF-2-AKT signaling and supports trabecular bone in glucocorticoid-induced osteoporosis.Stem cell reports · 2026Article
- Grx2 deficiency accelerates BMSC senescence and senile osteoporosis via CD36 S-glutathionylation.Cellular & molecular biology letters · 2026Article
- Review
- Targeting Endogenous Lipophagy: A Novel Strategy to Enhance MSC Osteogenesis and Mineralization for Senile Osteoporosis Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Gut Microbiota-Derived TMAO Drives MC3T3-E1 Senescence and Osteogenic Dysfunction via cGAS-STING-NF-κB Signaling: Implications for Age-Related Bone Loss.Calcified tissue international · 2026Article
- FTMT-mediated suppression of mitophagy links iron accumulation to osteoporosis.Redox biology · 2026Article
- Targeting Mitochondria in Aging-Related Diseases: Therapeutic Potential and Obstacles.MedComm · 2026Review
- Senescent BMSC-Derived Thbs1 Drives Inflammaging and Impairs Bone Regeneration by Suppressing PINK1/Parkin-Mediated Mitophagy in Macrophages.Aging cell · 2026Article
101 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Senile osteoporosis (SOP) is widely regarded as one of the typical aging-related diseases due to a decrease in bone mass and the destruction in microarchitecture. The inhibition of mitophagy can promote bone marrow mesenchymal stem cells (BMSCs) senescence, and increasing studies have shown that interventions targeting BMSCs senescence can ameliorate osteoporosis, exhibiting their potential for use as therapeutic strategies. Sirtuin-3 (Sirt3) is an essential mitochondria metabolic regulatory enzyme that plays an important role in mitochondrial homeostasis, but its role in bone homeostasis remains largely unknown. This study seeks to investigate whether advanced glycation end products (AGEs) accumulation aggravated BMSCs senescence and SOP, and explored the mechanisms underlying these effects. We observed that AGEs significantly aggravated BMSCs senescence, as well as promoted mitochondrial dysfunction and inhibited mitophagy in a concentration-dependent manner. In addition, this effect could be further strengthened by Sirt3 silencing. Importantly, we identified that the reduction of Sirt3 expression and the mitophagy were vital mechanisms in AGEs-induced BMSCs senescence. Furthermore, overexpression of Sirt3 by intravenously injection with recombinant adeno-associated virus 9 carrying Sirt3 plasmids (rAAV-Sirt3) significantly alleviated BMSCs senescence and the formation of SOP in SAMP6. In conclusion, our data demonstrated that Sirt3 protects against AGEs-induced BMSCs senescence and SOP. Targeting Sirt3 to improve mitophagy may represent a potential therapeutic strategy for attenuating AGEs-associated SOP.
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Registered trials
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.