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Table · dataset · 2026

Acupotomy Alleviates Knee Osteoarthritis by Regulating Chondrocyte Apoptosis via the IFT88-Mediated TRPV4 Signaling Axis

Listed in ZivaHub and Deakin Research Online and DMU Figshare and HKU DataHub and Swinburne Figshare and DaYta Ya Rona and SUNScholarData and figshare and Loughborough Research Repository and GRANTS Data and UP Research Data Repository — shown once because both records carry DOI 10.6084/m9.figshare.34033446.v1

<p dir="ltr">Knee osteoarthritis (KOA) is characterized by cartilage degeneration with no disease-modifying therapy available.

Description

Primary cilia, maintained by IFT88, regulate TRPV4-mediated calcium signaling in chondrocyte homeostasis, but their role in KOA remains unclear. Acupotomy shows clinical efficacy in KOA, yet its mechanism via this signaling axis is unknown.

This study investigated whether acupotomy alleviates KOA by regulating chondrocyte apoptosis through the IFT88-primary cilia-TRPV4 axis. Transcriptomic analysis, Lequesne MG scoring, Mankin scores,histology, electron microscopy, flow cytometry, immunoblotting, and qRT-PCR were performed on rabbit KOA models treated with acupotomy and/or the TRPV4 inhibitor HC067047. Transcriptomics identified 85 core reversal genes enriched in apoptosis, TRP channel regulation, ECM-receptor interaction, and PI3K-Akt pathways.

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Acupotomy improved Lequesne scores, cartilage pathology, and chondrocyte ultrastructure. Both acupotomy and HC067047 reduced elevated intracellular Ca²⁺, decreased calmodulin, and increased ACAN expression, with combination showing greatest effects. Both treatments reversed abnormal expression of Caspase-3, -9, -12, ACAN, COL2, and IFT88 at protein and mRNA levels, with greater combined effects in the combination group.

These findings suggest that acupotomy alleviates KOA in association with IFT88 upregulation and TRPV4-related signaling, which may contribute to reestablished calcium balance, suppressed calmodulin/caspase-mediated apoptosis, and promoted ECM synthesis. In conclusion, this study provides evidence supporting the IFT88–primary cilia–TRPV4 axis as a potential mechanism for acupotomy intervention in KOA. Acupotomy is associated with IFT88 upregulation and normalization of TRPV4-related signaling, which may contribute to restored calcium homeostasis, suppressed calmodulin/caspase-mediated apoptosis, and enhanced ACAN/COL2 matrix synthesis.</p>

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Inferred from text
Microscopy 75%
Provenance · 11 source records, 62 field assertions
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ZivaHuboai:figshare.com:article/3403344610 d agoJSON v1
Deakin Research Onlineoai:figshare.com:article/3403344610 d agoJSON v1
DMU Figshareoai:figshare.com:article/3403344610 d agoJSON v1
HKU DataHuboai:figshare.com:article/3403344610 d agoJSON v1
Swinburne Figshareoai:figshare.com:article/3403344610 d agoJSON v1
DaYta Ya Ronaoai:figshare.com:article/340334469 d agoJSON v1
SUNScholarDataoai:figshare.com:article/340334469 d agoJSON v1
figshareoai:figshare.com:article/340334469 d agoJSON v1
Loughborough Research Repositoryoai:figshare.com:article/340334469 d agoJSON v1
GRANTS Dataoai:figshare.com:article/340334469 d agoJSON v1
UP Research Data Repositoryoai:figshare.com:article/340334468 d agoJSON v1
FieldAssertionExtractorEvidence
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