ArticleJournal of orthopaedic translation2023
PINK1-mediated mitophagy contributes to glucocorticoid-induced cathepsin K production in osteocytes.
Article in Journal of orthopaedic translation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 19 citations in OpenAlex.
- Aptamer-functionalized tetrahedral framework nucleic acid delivery of siBhlhe22 for repairing osteoporotic bone defects via dual modulation of PI3K-Akt signaling and purine metabolism.Journal of nanobiotechnology · 2026Article
- Osteocytic Pink1/Prkn modulates M6P metabolism and contributes to GC-induced bone loss.Journal of orthopaedic translation · 2026Article
- Progress of Programmed Cell Death in Steroid-Induced Osteonecrosis of the Femoral Head.Orthopaedic surgery · 2026Review
- Advances in Research on Autophagy in Steroid-Induced Osteonecrosis of the Femoral Head: Dual Regulation of Its Beneficial and Detrimental Effects.Drug design, development and therapy · 2026Review
- Glucocorticoid-induced RPE injury in ARPE-19 cells: association with excessive autophagy and AMPK/mTOR signaling.International journal of ophthalmology · 2026Article
- GDF11 activates AMPK-dependent mitophagy to drive osteogenic differentiation of rat bone marrow mesenchymal stem cells.American journal of stem cells · 2026Article
- Relationship between cathepsin K and extracellular matrix dynamics: a comprehensive review.Frontiers in oncology · 2026Review
- Identification of biomarkers associated with mitophagy in bladder cancer.Scientific reports · 2025Article
- Effect of High Glucose and Carboxymethyl-Lysine on Osteocyte Gene Expression.American journal of molecular biology · 2025Article
- WAC Facilitates Mitophagy-mediated MSC Osteogenesis and New Bone Formation via Protecting PINK1 from Ubiquitination-Dependent Degradation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Application of collagen in bone regeneration.Journal of orthopaedic translation · 2025Review
- Prenatal hormone stress triggers embryonic cardiac hypertrophy outcome by ubiquitin-dependent degradation of mitochondrial mitofusin 2.iScience · 2024Article
- Mitochondrial dysfunction and therapeutic perspectives in osteoporosis.Frontiers in endocrinology · 2024Review
- Association BetweenPharmacogenomics and personalized medicine · 2023Article
- 2023 January issue Journal of Orthopaedic Translation.Journal of orthopaedic translation · 2023Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Glucocorticoid (GC) is one of frequently used anti-inflammatory agents, but its administration is unfortunately accompanied with bone loss. Although sporadic studies indicated that osteocytes are subject to a series of pathological changes under GC stress, including overexpression of cathepsin K, the definite role of osteocytes in GC-induced bone loss remains largely unclear. Methods: Gene expression of Results: GC triggered osteocytes to produce excessive cathepsin K which in turn led to the degradation of type I collagen in the extracellular matrix in a primary osteocyte Conclusion: GC-induced PINK1-mediated mitophagy substantially modulates the production of cathepsin K in osteocytes, which could be an underlying mechanism by which osteocytes contribute to the extracellular matrix degradation during bone loss. The Translational potential of this article: Findings of the current study indicate a possible role of osteocyte mitophagy in GC-induced bone loss, which provides a potential therapeutic approach to alleviate GC-induced osteoporosis by targeting PINK1-mediated osteocytic mitophagy.
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