ArticleArthritis research & therapy2019
Long non-coding RNA HOTAIR modulates intervertebral disc degenerative changes via Wnt/β-catenin pathway.
Article in Arthritis research & therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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48 citing papers in PubMed, 70 citations in OpenAlex.
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- Long non-coding RNA gene polymorphisms and risk of recurrent pregnancy loss: a meta-analysis.Journal of assisted reproduction and genetics · 2026Review
- Epigenetic research methods and animal models for intervertebral disc degeneration (Review).Molecular medicine reports · 2026Review
- Resetting the epigenetic clock: cellular senescence and regenerative strategies in intervertebral disc degeneration.Frontiers in aging · 2026Review
- Cellular and molecular mechanisms of diabetes-mediated disc degeneration.Frontiers in endocrinology · 2026Review
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- Transcriptomic insights into the anti-apoptotic effect of Tuina in rabbit model of intervertebral disc degeneration.Journal of orthopaedic surgery and research · 2025Article
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- Research progress on long non‑coding RNAs in non‑infectious spinal diseases (Review).Molecular medicine reports · 2024Review
- S100A6 Regulates nucleus pulposus cell apoptosis via Wnt/β-catenin signaling pathway: an in vitro and in vivo study.Molecular medicine (Cambridge, Mass.) · 2024Article
- Progress in regulating inflammatory biomaterials for intervertebral disc regeneration.Bioactive materials · 2024Review
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- High-Tech Methods of Cytokine Imbalance Correction in Intervertebral Disc Degeneration.International journal of molecular sciences · 2023Review
- Cytokine Imbalance as a Biomarker of Intervertebral Disk Degeneration.International journal of molecular sciences · 2023Review
- Regulatory Effect of Inflammatory Mediators in Intervertebral Disc Degeneration.Mediators of inflammation · 2023Review
- Regulatory roles of noncoding RNAs in intervertebral disc degeneration as potential therapeutic targets (Review).Experimental and therapeutic medicine · 2023Review
- The regulatory role and therapeutic application of pyroptosis in musculoskeletal diseases.Cell death discovery · 2022Review
- Article
- Targeting Autophagy for Developing New Therapeutic Strategy in Intervertebral Disc Degeneration.Antioxidants (Basel, Switzerland) · 2022Review
- p300 arrests intervertebral disc degeneration by regulating the FOXO3/Sirt1/Wnt/β-catenin axis.Aging cell · 2022Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
backgroundIntervertebral disc degeneration (IDD) has a complicated and enigmatic pathogenic process. Accumulating evidence shows that long non-coding RNAs (LncRNAs) play a role in the pathogenesis of IDD. This study aimed to investigate the expression and role of the LncRNA HOTAIR in IDD pathogenesis.
methodsNucleus pulposus (NP) tissue samples from 10 patients with idiopathic scoliosis and 10 patients with lumbar disc herniation were collected. qRT-PCR was used to assess the expression of HOTAIR and ECM-related genes; western blotting was used to detect the expression of senescence biomarkers, apoptosis-related proteins, and Wnt/β-catenin pathway; flow cytometry was used to detect apoptosis; and the MTT assay was used to determine cell proliferation. Moreover, a classic needle-punctured rat tail model was used to investigate the role of HOTAIR in IDD in vivo.
resultsThe results showed that the expression of HOTAIR significantly increased during IDD progression. The overexpression of HOTAIR was found to induce nucleus pulposus (NP) cell senescence, apoptosis, and extracellular matrix (ECM) degradation. HOTAIR silencing by RNA interference in NP cells prevented interleukin-1β-induced NP cell senescence, apoptosis, and ECM degradation. Furthermore, we found that the Wnt/β-catenin pathway played a role in regulating HOTAIR to induce these changes in NP cells. Moreover, HOTAIR inhibition in a rat model effectively attenuated IDD symptoms in vivo.
conclusionsOur findings confirmed that HOTAIR promoted NP cell senescence, apoptosis, and ECM degradation via the activation of the Wnt/β-catenin pathway, while silencing HOTAIR attenuated this degeneration process, indicating a potential therapeutic target against IDD.
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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.