ArticleiScience2025
The inhibition of PINK1/Drp1-mediated mitophagy by hyperglycemia leads to impaired osteoblastogenesis in diabetes.
Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed.
- Review
- Orchestrated Engineered Polyphenol-Peptide Condensates Coupled With β-GP Reverses Diabetic Osteoporosis by Remodeling Mitophagy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Targeting Mitochondria in Aging-Related Diseases: Therapeutic Potential and Obstacles.MedComm · 2026Review
- Traditional Chinese medicine-derived monomers improve bone metabolic imbalance and delay osteoporosis progression by regulating mitochondrial homeostasis.Frontiers in cell and developmental biology · 2026Review
- Research progress on the association of maternal high-fat diet with offspring neurodevelopment and susceptibility to Parkinson's disease.Frontiers in nutrition · 2026Review
- GDF11 activates AMPK-dependent mitophagy to drive osteogenic differentiation of rat bone marrow mesenchymal stem cells.American journal of stem cells · 2026Article
- An emerging role of mitochondrial quality control in bone metabolism: from molecular mechanisms to targeted therapeutic interventions.Cellular and molecular life sciences : CMLS · 2025Review
- Caffeine intake is inversely associated with osteoporosis risk based on cross-sectional and genetic evidence.Scientific reports · 2025Article
- New Evidence, Creative Insights, and Strategic Solutions: Advancing the Understanding and Practice of Diabetes Osteoporosis.Journal of diabetes · 2025Review
- Mitochondria: a key regulator of programmed cell death in OP.Frontiers in endocrinology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Impaired bone quality and increased fracture risk are cardinal features of the skeleton in diabetes mellitus. Hyperglycemia-induced oxidative stress is proposed as a potential underlying mechanism, but the precise pathogenic mechanism remains incompletely understood. In this investigation, osteoblasts under high glucose exhibited heightened levels of reactive oxygen species, impaired mitochondrial membrane potential, and profound inhibition of late-stage osteoblast differentiation. Further analyses uncovered that high glucose resulted in the downregulation of the PINK1/Drp1 pathway in osteoblasts, consequently leading to impaired mitophagy. Conversely, the upregulation of PINK1/Drp1 pathway activated mitophagy, which restored the differentiation capacity of osteoblasts. Notably, in an STZ-induced diabetic mouse model, BMP9 upregulated the expression of PINK1/Drp1 in the bone tissue, leading to an improvement in bone quality and bone mineral density. These findings suggest that the PINK1/Drp1 pathway might be a potential therapeutic target to enhance osteogenic differentiation and treat diabetic osteoporosis.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.