ReviewAnnals of medicine2026
Mechanisms and therapeutic potential of mitochondrial-targeted therapies in bone repair.
Review in Annals of medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Promoting Bone Health in Layer Chickens from the Perspective of Mitochondrial Energy Metabolism in Osteoclasts.Animals : an open access journal from MDPI · 2026Review
- Metformin as a Metabolic Reprogramming Interface in Host-Pathogen and Bone Microenvironment Crosstalk: A Dual-Target Strategy Against Antimicrobial Resistance and Osteoporotic Bone Loss.Antibiotics (Basel, Switzerland) · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bone defect repair remains a significant challenge in orthopedics, particularly for critical-sized bone defects, which often result in nonunion. Traditional treatments have numerous limitations. Recent studies have highlighted the pivotal role of mitochondria as cellular energy and metabolic hubs influencing the function of osteoblasts, osteoclasts, and chondrocytes. Mitochondria regulate energy metabolism, ROS signaling, mitochondrial dynamics, and apoptosis, all of which are essential for maintaining proper bone function. Mitochondrial dysfunction has been identified as a key intrinsic factor contributing to the failure of bone repair. Thus, targeting mitochondria has emerged as a promising therapeutic strategy. This article systematically reviewed the various functional roles of mitochondria in bone repair and evaluated the current progress of mitochondrial-targeted therapeutic strategies. We focused on the mechanisms of action and preclinical advancements related to small molecule compounds, functionalized biomaterials, and advanced cell therapies, offering a theoretical foundation for their potential clinical application. Mitochondrial-targeted therapies show significant promise for enhancing bone repair by improving cellular energy metabolism, restoring redox homeostasis, optimizing mitochondrial quality control, and promoting cell survival. However, this field faces several challenges, including improving targeted delivery efficiency, ensuring long-term safety, and translating these strategies into clinical practice. Future research should prioritize the development of more precise delivery technologies, exploration of multi-target synergistic approaches, and rigorous clinical trials to support the practical application of mitochondrial-targeted therapies for clinical bone regeneration.
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What OpenQuestion 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 OpenQuestion graph.