ArticleMolecular therapy. Nucleic acids2022
CRISPR-Cas9-mediated loss of function of β-catenin attenuates intervertebral disc degeneration.
Article in Molecular therapy. Nucleic acids, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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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.
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Who cites it
18 citing papers in PubMed, 18 citations in OpenAlex.
- Surviving the Nucleus Pulposus Desert: Next-Generation Strategies for Intervertebral Disc Cell Therapy.JOR spine · 2026Article
- Stem cell therapy for degenerative disc disease: A systematic review of preclinical evidence, clinical translation, and future directions.North American Spine Society journal · 2026Review
- Intervertebral disc degeneration.Nature reviews. Disease primers · 2026Review
- SPP1 in notochord cells modulates intervertebral disc degeneration through CD44 recognition by macrophages based on single-cell transcriptome analysis.International journal of surgery (London, England) · 2026Article
- Bioactive Therapies for Degenerative Disc Disease: Challenges and Innovations.World neurosurgery · 2025Article
- Harnessing CRISPR potential for intervertebral disc regeneration strategies.Frontiers in bioengineering and biotechnology · 2025Review
- Immune microenvironment in intervertebral disc degeneration: pathophysiology and therapeutic potential.Frontiers in immunology · 2025Review
- Advancing Pain Understanding and Drug Discovery: Insights from Preclinical Models and Recent Research Findings.Pharmaceuticals (Basel, Switzerland) · 2024Review
- CRISPR-mediated Sox9 activation and RelA inhibition enhance cell therapy for osteoarthritis.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Progress of Gene-Functionalized Regenerative Material Repair Intervertebral Disc Degeneration.Small science · 2024Article
- Nerve growth factor receptor limits inflammation to promote remodeling and repair of osteoarthritic joints.Nature communications · 2024Article
- Potential therapeutic strategies for osteoarthritis via CRISPR/Cas9 mediated gene editing.Reviews in endocrine & metabolic disorders · 2024Review
- Intervertebral disc-intrinsic Hedgehog signaling maintains disc cell phenotypes and prevents disc degeneration through both cell autonomous and non-autonomous mechanisms.Cellular and molecular life sciences : CMLS · 2024Article
- Engineering approaches for RNA-based and cell-based osteoarthritis therapies.Nature reviews. Rheumatology · 2024Review
- Nerve Growth Factor Receptor Limits Inflammation to Promote Remodeling and Repair of Osteoarthritic Joints.bioRxiv : the preprint server for biology · 2023Article
- Loss of miR-204 and miR-211 shifts osteochondral balance and causes temporomandibular joint osteoarthritis.Journal of cellular physiology · 2023Article
- Review
- Intervertebral disc degeneration-Current therapeutic options and challenges.Frontiers in public health · 2023Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Intervertebral disc degeneration is a very common medical condition causing pain and disability, and it cannot be reversed by available treatment options. Here we report that targeting β-catenin, a pivotal factor associated with disc degeneration, ameliorates disc degeneration in a mouse model of disc injury. Degenerative changes in the disc in response to disc injury include decompression of nucleus pulposus (NP), replacement of notochordal cells in the NP by chondrocyte-like cells, and disorganization of annulus fibrosus (AF). Importantly, downregulation of β-catenin through intradiscal injection of CRISPR-Cas9-expressing adeno-associated virus significantly mitigated all these pathological changes, by preserving notochordal cells and attenuating chondro-osteogenesis in the NP, as well as maintaining the AF structure. Moreover, β-catenin loss-of-function decelerated the rapid induction of catabolic reactions in disc matrix and attenuated pain-related neural events during disc degeneration. Thus, our data demonstrate that targeting β-catenin in disc cells through CRISPR-Cas9 has multifaceted therapeutic effects on disc degeneration, and we suggest that β-catenin plays a fundamental role in the remodeling and degenerative processes of the disc. In addition, this study proposes that CRISPR-Cas9 is a useful tool for identifying new drug targets and developing therapeutic strategies for disc degeneration.
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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.