ArticleAging2021
Circular RNA ITCH promotes extracellular matrix degradation via activating Wnt/β-catenin signaling in intervertebral disc degeneration.
Article in Aging, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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
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Who cites it
24 citing papers in PubMed, 31 citations in OpenAlex.
- Single-cell and spatial transcriptomics characterisation of RSPO2Journal of orthopaedic translation · 2026Article
- Metabolic reprogramming in intervertebral disc degeneration: mechanisms and therapeutic opportunities.Frontiers in cell and developmental biology · 2026Review
- Gastrodin Alleviates Lumbar Intervertebral Disc Degeneration by Suppressing the NF-κB and MAPK Pathways.Cell biochemistry and biophysics · 2025Article
- SOX4 accelerates intervertebral disc degeneration via EZH2/NRF2 pathway in response to mitochondrial ROS-dependent NLRP3 inflammasome activation in nucleus pulposus cells.Journal of translational medicine · 2025Article
- EZH2-H3K27me3-Mediated Epigenetic Silencing of DKK1 Induces Nucleus Pulposus Cell Pyroptosis in Intervertebral Disc Degeneration by Activating NLRP3 and NAIP/NLRC4.Inflammation · 2025Article
- ZIP8 Regulates Inflammation and Macrophage Polarisation in Intervertebral Disc Degeneration via the Wnt/β-Catenin Pathway.Journal of cellular and molecular medicine · 2025Article
- Bioinformatics and Experimental Validation of FLVCR1 and SOX4 in Regulating Mitochondria-Macrophage Crosstalk in Disc Degeneration.Journal of inflammation research · 2025Article
- Role of Circular RNAs in Prostate Cancer.Current medicinal chemistry · 2024Review
- The pathological mechanisms of circRNAs in mediating intervertebral disc degeneration.Non-coding RNA research · 2023Review
- Loss of Pinch Proteins Causes Severe Degenerative Disc Disease-Like Lesions in Mice.Aging and disease · 2023Article
- Review
- N6-methyladenosine hypomethylation of circGPATCH2L regulates DNA damage and apoptosis through TRIM28 in intervertebral disc degeneration.Cell death and differentiation · 2023Article
- Circ-STC2 promotes the ferroptosis of nucleus pulposus cells via targeting miR-486-3p/TFR2 axis.Journal of orthopaedic surgery and research · 2023Article
- Circular RNA and intervertebral disc degeneration: unravelling mechanisms and implications.Frontiers in molecular biosciences · 2023Review
- Circular RNAs: typical biomarkers for bone-related diseases.Journal of Zhejiang University. Science. B · 2022Article
- Circ0007042 alleviates intervertebral disc degeneration by adsorbing miR-369 to upregulate BMP2 and activate the PI3K/AKt pathway.Arthritis research & therapy · 2022Article
- CRISPR-Cas9-mediated loss of function of β-catenin attenuates intervertebral disc degeneration.Molecular therapy. Nucleic acids · 2022Article
- Hsa_circ_0134111 promotes intervertebral disc degeneration via sponging miR-578.Cell death discovery · 2022Article
- CircRNA ITCH: Insight Into Its Role and Clinical Application Prospect in Tumor and Non-Tumor Diseases.Frontiers in genetics · 2022Review
- Circ_0005918 Sponges miR-622 to Aggravate Intervertebral Disc Degeneration.Frontiers in cell and developmental biology · 2022Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intervertebral disc degeneration (IDD) is the prevailing spine disorder and is associated with musculoskeletal disease. The extracellular matrix (ECM) degradation is an essential hallmark of IDD progression. Circular RNAs (circRNAs), as crucial cellular regulators, participate in multiple pathological processes including IDD. Here, we tried to explore the effect of circITCH on the ECM degradation of IDD and the underlying mechanism. Significantly, the expression levels of circITCH were elevated in the IDD patients' nucleus pulposus (NP) tissues relative to that of normal cases. CircITCH promoted apoptosis and decreased proliferation of NP cells. CircITCH contributed to ECM degradation, as demonstrated by increased ADAMTS4 and MMP13 expression and decreased aggrecan and collagen II expression. Mechanically, miR-17-5p could be sponged by circITCH and miR-17-5p inhibited ECM degradation by repressing SOX4 in degenerative NP cells. CircITCH could activate Wnt/β-catenin pathway by targeting miR-17-5p/SOX4 signaling. SOX4 overexpression, miR-17-5p inhibitor, or Wnt/β-catenin signaling activator LiCl was able to reverse circITCH knockdown-inhibited apoptosis and ECM degradation, and circITCH knockdown-enhanced proliferation in NP cells. Thus, we conclude that circITCH promotes ECM degradation in IDD by activating Wnt/β-catenin through miR-17-5p/SOX4 signaling. Our finding presents novel insight into the mechanism that circITCH modulates the IDD progression. CircITCH and SOX4 may serve as potential targets for IDD therapy.
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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.