ReviewBiomolecules2022
Mitophagy-A New Target of Bone Disease.
Review in Biomolecules, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.
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
42 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.
- Advances in research on the relationship between mitochondrial dysfunction and osteoporosis: a bibliometric study from 2014 to 2024.Frontiers in medicine · 2025Pooled it
- PINK1 deficiency exacerbates age-related bone loss in association with enhanced inflammatory adipocyte differentiation.Genes & diseases · 2027Article
- Mechanisms and therapeutic potential of mitochondrial-targeted therapies in bone repair.Annals of medicine · 2026Review
- CBX3 aggravates nucleus pulposus cell apoptosis and extracellular matrix degradation in vitro via repressing SESN2-mediated mitophagy in an H3K9me3-dependent manner.Molecular biology reports · 2026Article
- Bone organoids and mitochondrial reprogramming.Journal of orthopaedic translation · 2026Review
- Exercise-Induced Regulation of Bone Remodeling via Mitophagy: A Review of Current Evidence.Biomolecules · 2026Review
- Mitochondrial Regulation of Periodontal Ligament Stem Cell Fate and Function.Stem cell reviews and reports · 2026Review
- Synovial microenvironment and fluorescence imaging for early rheumatoid arthritis diagnosis.Journal of pharmaceutical analysis · 2026Review
- Elucidation of ACAT1's role in hepatic ischemia-reperfusion injury: TFEB-mediated mitophagy and ferroptosis modulation as therapeutic targets.Journal of pharmaceutical analysis · 2026Article
- Systematic analysis of the mitophagy scoring system in the prognosis and immunotherapy of HCC patients.Discover oncology · 2026Article
- Lactylation Reprogramming in the Bone Infection Microenvironment Identifies PGK1 K361 as a Potential Therapeutic Target for Osteogenic Dysfunction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Article
- The multifaceted functions of selective autophagy in cancer: molecular basis, consequences, and clinical prospects.Molecular cancer · 2026Review
- Osteoarthritis: molecular pathogenesis and potential therapeutic options.Signal transduction and targeted therapy · 2026Review
- USP34 attenuates cartilage degradation in temporomandibular joint osteoarthritis by ANT1-mediated mitophagy.JBMR plus · 2026Article
- Targeting mitochondrial oxidative stress: A novel therapeutic strategy for degenerative joint diseases (Review).Biomedical reports · 2026Review
- Spatio-temporal dynamics of autophagy-associated genes in macrophage-driven atherosclerosis: an integrated omics and experimental study.Frontiers in endocrinology · 2026Article
- Curcumin-preconditioned bone marrow mesenchymal stem cell exosomes ameliorate postmenopausal osteoporosis by activating mitophagy in osteoblast-lineage cells.Frontiers in cell and developmental biology · 2026Article
- Traditional Chinese medicine-derived monomers improve bone metabolic imbalance and delay osteoporosis progression by regulating mitochondrial homeostasis.Frontiers in cell and developmental biology · 2026Review
- Melatonin Supplementation Relieves Fluoride-Induced Bone Injury via Ion Homeostasis Disorder and PINK1/Parkin-Mediated Mitophagy.Foods (Basel, Switzerland) · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bone diseases are usually caused by abnormal metabolism and death of cells in bones, including osteoblasts, osteoclasts, osteocytes, chondrocytes, and bone marrow mesenchymal stem cells. Mitochondrial dysfunction, as an important cause of abnormal cell metabolism, is widely involved in the occurrence and progression of multiple bone diseases, including osteoarthritis, intervertebral disc degeneration, osteoporosis, and osteosarcoma. As selective mitochondrial autophagy for damaged or dysfunctional mitochondria, mitophagy is closely related to mitochondrial quality control and homeostasis. Accumulating evidence suggests that mitophagy plays an important regulatory role in bone disease, indicating that regulating the level of mitophagy may be a new strategy for bone-related diseases. Therefore, by reviewing the relevant literature in recent years, this paper reviews the potential mechanism of mitophagy in bone-related diseases, including osteoarthritis, intervertebral disc degeneration, osteoporosis, and osteosarcoma, to provide a theoretical basis for the related research of mitophagy in bone diseases.
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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.