ReviewRedox biology2025
Impact of reactive oxygen species on bone regeneration in diabetes: Mechanisms and therapeutic strategies.
Review in Redox biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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
6 citing papers in PubMed.
- An Inulin-Type Atractylodes Macrocephala Polysaccharide Alleviates Weightlessness-Induced Bone Loss in Association with the Nrf2/HO-1 Pathway.Nutrients · 2026Article
- Promoting Bone Health in Layer Chickens from the Perspective of Mitochondrial Energy Metabolism in Osteoclasts.Animals : an open access journal from MDPI · 2026Review
- pH-Responsive mPEG-PLGA/Dexamethasone Coatings for Corrosion Control and Osteo-Immune Modulation of Biodegradable Magnesium.Polymers · 2026Article
- The cutting-edge advancements in biomaterials under the guidance of intelligence and bionics.Regenerative biomaterials · 2026Review
- Injectable Mn-Icariin-functionalized silk fibroin/PEG hydrogels restore redox homeostasis and reprogram osteogenic-angiogenic coupling for diabetic bone regeneration.Regenerative biomaterials · 2026Article
- Strontium-baicalein coated β-tricalcium phosphate scaffold enhances diabetic bone regeneration via synergistic ROS scavenging and osteogenic activation.Regenerative biomaterials · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic bone regeneration is significantly affected by reactive oxygen species (ROS)-induced oxidative stress (OS), which disrupts the balance between osteoclast (OC)-mediated resorption and osteoblast (OB)-mediated formation of bone tissue. This review synthesizes current understanding of how hyperglycemia-driven ROS overproduction dysregulates OB and OC functions, leading to pathological bone remodeling and compromised healing. The key molecular mechanisms involved, such as RANK/RANKL, NF-κB, and MAPK, are discussed, highlighting their role in the ROS-mediated feedback loop that promotes OC differentiation while inhibiting OB survival, differentiation, and activity, worsening bone degeneration. Furthermore, the review addresses ROS-induced cell death pathways (apoptosis, ferroptosis, necroptosis, pyroptosis) along with the pathophysiological changes in the bone marrow microenvironment. Emerging therapeutic strategies to reduce oxidative damage, including antioxidant (AO) therapies and innovative drug delivery systems, offer promise for restoring bone regenerative capacity in diabetic conditions. These innovations aim to restore redox homeostasis, mitigate OS damage, and reactivate endogenous bone regenerative capacity. Understanding these mechanisms provides a foundation for developing targeted interventions to improve clinical outcomes in diabetic bone disease.
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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.