ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2020
Aging aggravates intervertebral disc degeneration by regulating transcription factors toward chondrogenesis.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 47 citations in OpenAlex.
- β-Catenin-Deficient Intervertebral Disc Cells Reduce Chemotactic Transcription and Myeloid Cell Recruitment to Injured Discs of Mice.Aging cell · 2026Article
- Increased angiogenesis-osteogenesis coupling in the endplate at early stages of intervertebral disc degeneration.Scientific reports · 2026Article
- Macrophage Changes and High-Throughput Sequencing in Aging Mouse Intervertebral Disks.JOR spine · 2025Article
- ATF1 and miR-27b-3p drive intervertebral disc degeneration through the PPARG/NF-κB signaling axis.Communications biology · 2025Article
- Unveiling the role of TCF19 in intervertebral disc degeneration with single-cell and bulk RNA sequencing.Scientific reports · 2025Article
- Exploring the correlation between magnetic resonance diffusion tensor imaging (DTI) parameters and aquaporin expression and biochemical composition content in degenerative intervertebral disc nucleus pulposus tissue: a clinical experimental study.BMC musculoskeletal disorders · 2025Article
- Osteoporosis treatments for intervertebral disc degeneration and back pain: a perspective.JBMR plus · 2024Article
- Bushen Huoxue Formula Inhibits IL-1β-Induced Apoptosis and Extracellular Matrix Degradation in the Nucleus Pulposus Cells and Improves Intervertebral Disc Degeneration in Rats.Journal of inflammation research · 2024Article
- Emerging role and therapeutic implications of p53 in intervertebral disc degeneration.Cell death discovery · 2023Review
- Loss of Pinch Proteins Causes Severe Degenerative Disc Disease-Like Lesions in Mice.Aging and disease · 2023Article
- Review
- Oxidative stress in intervertebral disc degeneration: Molecular mechanisms, pathogenesis and treatment.Cell proliferation · 2023Review
- Article
- Smoking and tetramer tryptase accelerate intervertebral disc degeneration by inducing METTL14-mediated DIXDC1 mMolecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- ERBB2-PTGS2 axis promotes intervertebral disc degeneration by regulating senescence of nucleus pulposus cells.BMC musculoskeletal disorders · 2023Article
- Review
- Human Embryonic Stem-Cell-Derived Exosomes Repress NLRP3 Inflammasome to Alleviate Pyroptosis in Nucleus Pulposus Cells by Transmitting miR-302c.International journal of molecular sciences · 2023Article
- mTOR is involved in LRP5-induced osteogenic differentiation of normal and aged periodontal ligament stem cells in vitro.Journal of molecular histology · 2022Article
- Suppression of Sost/Sclerostin and Dickkopf-1 Augment Intervertebral Disc Structure in Mice.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2022Article
- Development, Pathogenesis, and Regeneration of the Intervertebral Disc: Current and Future Insights Spanning Traditional to Omics Methods.Frontiers in cell and developmental biology · 2022Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Osterix is a critical transcription factor of mesenchymal stem cell fate, where its loss or loss of Wnt signaling diverts differentiation to a chondrocytic lineage. Intervertebral disc (IVD) degeneration activates the differentiation of prehypertrophic chondrocyte-like cells and inactivates Wnt signaling, but its interactive role with osterix is unclear. First, compared to young-adult (5 mo), mechanical compression of old (18 mo) IVD induced greater IVD degeneration. Aging (5 vs 12 mo) and/or compression reduced the transcription of osterix and notochordal marker T by 40-75%. Compression elevated the transcription of hypertrophic chondrocyte marker MMP13 and pre-osterix transcription factor RUNX2, but less so in 12 mo IVD. Next, using an Ai9/td reporter and immunohistochemical staining, annulus fibrosus and nucleus pulposus cells of young-adult IVD expressed osterix, but aging and compression reduced its expression. Lastly, in vivo LRP5-deficiency in osterix-expressing cells inactivated Wnt signaling in the nucleus pulposus by 95%, degenerated the IVD to levels similar to aging and compression, reduced the biomechanical properties by 45-70%, and reduced the transcription of osterix, notochordal markers and chondrocytic markers by 60-80%. Overall, these data indicate that age-related inactivation of Wnt signaling in osterix-expressing cells may limit regeneration by depleting the progenitors and attenuating the expansion of chondrocyte-like cells.
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