Evidence map›Paper›PMID 36474855›Full record

ArticleJournal of orthopaedic translation2023

PINK1-mediated mitophagy contributes to glucocorticoid-induced cathepsin K production in osteocytes.

Jun Yuan, You-Shui Gao, De-Lin Liu, Andrew Chi Pang Tai, Hong Zhou, John M Papadimitriou, Chang-Qing Zhang, Ming-Hao Zheng, Jun-Jie Gao

Open access · goldAbstract read
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.4field-weighted citation impact, top 19% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
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  9. Article
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  11. Application of collagen in bone regeneration.Journal of orthopaedic translation · 2025
    Review
  12. Article
  13. Review
  14. Association BetweenPharmacogenomics and personalized medicine · 2023
    Article
  15. 2023 January issue Journal of Orthopaedic Translation.Journal of orthopaedic translation · 2023
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 2 countries.

Jun YuanCentre for Orthopaedic Translational Research, Medical School, The University of Western Australia, Nedlands, Western Australia, 6009, Australia.
You-Shui GaoDepartment of Orthopaedic Surgery, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, 200233, China.
De-Lin LiuCentre for Orthopaedic Translational Research, Medical School, The University of Western Australia, Nedlands, Western Australia, 6009, Australia.
Andrew Chi Pang TaiCentre for Orthopaedic Translational Research, Medical School, The University of Western Australia, Nedlands, Western Australia, 6009, Australia.
Hong ZhouBone Research Program, ANZAC Research Institute, The University of Sydney, Sydney, NSW, Australia.
John M PapadimitriouPathwest Laboratories and Faculty of Health and Medical Sciences, The University of Western Australia, Nedlands, WA, 6009, Australia.
Chang-Qing ZhangDepartment of Orthopaedic Surgery, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, 200233, China.
Ming-Hao ZhengCentre for Orthopaedic Translational Research, Medical School, The University of Western Australia, Nedlands, Western Australia, 6009, Australia.
Jun-Jie GaoDepartment of Orthopaedic Surgery, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, 200233, China.
The University of Western Australia · AUShanghai Jiao Tong University · CNThe University of Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

Cathepsin KCCCP, Carbonyl cyanide chlorophenylhydrazoneCTSK, cathepsin KCTX, carboxyterminal telopeptide of type I collagenDrp1, dynamin-related protein 1GC, glucocorticoidGlucocorticoidMfn2, mitofusin-2MitophagyMTR, MitoTracker RedOsteocytePINK1PINK1, PTEN-induced putative kinase 1TFEB, transcription factor EBTRAP, tartrate-resistant acid phosphataseΔѰm, mitochondria membrane potential

Identifiers

PMID36474855
PMCPMC9708541
OpenAlexW4310186726

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.