ReviewFrontiers in endocrinology2024
Mitochondrial dysfunction and therapeutic perspectives in osteoporosis.
Review in Frontiers in endocrinology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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The trial behind it
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Who cites it
46 citing papers in PubMed, 43 citations in OpenAlex.
- Immunometabolic Remodeling in Osteosarcopenia: Inflammaging, Mitochondrial Dysfunction, Gut-Derived Metabolites and Therapeutic Opportunities.Metabolites · 2026Review
- Tri-modal nanocatalytic microenvironment regulations for macrophage reprogramming and osteoporotic fracture healing promotion.Materials today. Bio · 2026Article
- 17β-Estradiol Maintains Mitochondrial Homeostasis in Osteoblasts by Inhibiting MMP-8 and Activating the Ras Signaling Pathway in Postmenopausal Osteoporosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Free mitochondrial transfer enhances bone regeneration through cathepsin H mediated cysteine cycle.Cell communication and signaling : CCS · 2026Article
- Therapeutic effect of mitochondrial transfer on bone tissue diseases: treatment strategy of mitochondrial transplantation and delivery technology.Journal of orthopaedic translation · 2026Review
- Mechanistic Links Underlying the Comorbidity of Osteoporosis and Osteoarthritis: Cell Fate Plasticity Driven by the Subchondral Bone Microenvironment.International journal of molecular sciences · 2026Review
- Targeting NSignal transduction and targeted therapy · 2026Article
- Regulating Glucose Metabolism Enzymes for Osteoporosis Therapy: Current and Future Approaches.International journal of molecular sciences · 2026Review
- Identification of a Novel Mitochondrial-Related Gene Signature for BMSCs in Osteoporosis Combining Single-Cell and Bulk Transcriptome Data.Biochemical genetics · 2026Article
- Three-dimensional (3D) culture-primed placental mesenchymal stem cells decrease cellular heterogeneity, significantly enhancing osteogenesis via improving mitochondrial function.Materials today. Bio · 2026Article
- The purinergic receptor P2rx7 mediated ATP sensing is required to prevent bone aging by directing mitochondrial fitness of MSCs.Journal of advanced research · 2026Article
- The pivotal role of mitochondria in osteoporosis: From pathogenesis to future therapies.Biochemistry and biophysics reports · 2026Review
- Aging-Driven Inter-Organ Crosstalk in Postmenopausal Osteoporosis: From Immunometabolic Drift to Multisystem Frailty.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
- ANGPTL8 accelerates bone loss in diabetic mice by promoting osteoclastic differentiation and inhibiting osteoblastic differentiation through AMPK pathway-mediated metabolic reprogramming.Cellular and molecular life sciences : CMLS · 2026Article
- Unraveling the telomere-mitochondrial axis in colorectal cancer: Results from a prospectively followed cohort.Molecular medicine (Cambridge, Mass.) · 2026Article
- Cuproptosis and Diabetic Osteoporosis: Mechanisms and Therapeutic Prospects.International journal of molecular sciences · 2026Review
- Targeting ferroptosis in osteoporosis: mechanisms and natural products therapies.Frontiers in pharmacology · 2026Review
- Exploratory analysis of mitochondrial transcription factor A as a putative biomarker for osteoporosis: a cross-sectional study.Frontiers in endocrinology · 2026Article
- Regulation of Mitochondrial Homeostasis: Applications of Nanobiomaterials in Age-Related Bone Diseases.International journal of nanomedicine · 2026Review
- Targeting a Shared Mitophagy Regulator: The SIRT1-FOXO3-DEPP1 Axis Underpins the Dual Bone and Brain Benefits of Total Flavonoids fromResearch (Washington, D.C.) · 2026Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoporosis (OP) is a systemic skeletal disorder characterized by reduced bone mass and structural deterioration of bone tissue, resulting in heightened vulnerability to fractures due to increased bone fragility. This condition primarily arises from an imbalance between the processes of bone resorption and formation. Mitochondrial dysfunction has been reported to potentially constitute one of the most crucial mechanisms influencing the pathogenesis of osteoporosis. In essence, mitochondria play a crucial role in maintaining the delicate equilibrium between bone formation and resorption, thereby ensuring optimal skeletal health. Nevertheless, disruption of this delicate balance can arise as a consequence of mitochondrial dysfunction. In dysfunctional mitochondria, the mitochondrial electron transport chain (ETC) becomes uncoupled, resulting in reduced ATP synthesis and increased generation of reactive oxygen species (ROS). Reinforcement of mitochondrial dysfunction is further exacerbated by the accumulation of aberrant mitochondria. In this review, we investigated and analyzed the correlation between mitochondrial dysfunction, encompassing mitochondrial DNA (mtDNA) alterations, oxidative phosphorylation (OXPHOS) impairment, mitophagy dysregulation, defects in mitochondrial biogenesis and dynamics, as well as excessive ROS accumulation, with regards to OP (
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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.