ArticleScientific reports2019
Caspase-3 knockout inhibits intervertebral disc degeneration related to injury but accelerates degeneration related to aging.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 37 citations in OpenAlex.
- Regulated cell death in musculoskeletal development, homeostasis, and diseases.Fundamental research · 2026Review
- Therapeutic strategies for intervertebral disc degeneration: Extracellular vesicles and microRNAs derived from mesenchymal stem cells.World journal of stem cells · 2025Review
- Exploring the therapeutic potential of puerarin on intervertebral disc degeneration by regulating apoptosis of nucleus pulposus cells.JOR spine · 2024Article
- Reverse Translational Approach Using Biomaterials and Stem Cells for Intervertebral Disc Degeneration.JMA journal · 2024Article
- Bioinformatics-based discovery of intervertebral disc degeneration biomarkers and immune-inflammatory infiltrates.JOR spine · 2024Article
- Review
- The mechanism by which Naru 3 pill protects against intervertebral disc cartilage endplate degeneration based on network pharmacology and experimental verification.Journal of orthopaedic surgery and research · 2023Article
- Strontium Attenuates Hippocampal Damage via Suppressing Neuroinflammation in High-Fat Diet-Induced NAFLD Mice.International journal of molecular sciences · 2023Article
- Intervertebral disc cell fate during aging and degeneration: apoptosis, senescence, and autophagy.North American Spine Society journal · 2023Article
- Nimbolide targeting SIRT1 mitigates intervertebral disc degeneration by reprogramming cholesterol metabolism and inhibiting inflammatory signaling.Acta pharmaceutica Sinica. B · 2023Article
- GLUT1 is redundant in hypoxic and glycolytic nucleus pulposus cells of the intervertebral disc.JCI insight · 2023Article
- Review
- Knockdown of triggering receptor expressed on myeloid cells 1 (TREM1) inhibits endoplasmic reticulum stress and reduces extracellular matrix degradation and the apoptosis of human nucleus pulposus cells.Experimental and therapeutic medicine · 2022Article
- Targeting Autophagy for Developing New Therapeutic Strategy in Intervertebral Disc Degeneration.Antioxidants (Basel, Switzerland) · 2022Review
- Causes of and Molecular Targets for the Treatment of Intervertebral Disc Degeneration: A Review.Cells · 2022Review
- Development, Pathogenesis, and Regeneration of the Intervertebral Disc: Current and Future Insights Spanning Traditional to Omics Methods.Frontiers in cell and developmental biology · 2022Review
- Circular RNAs in Intervertebral Disc Degeneration: An Updated Review.Frontiers in molecular biosciences · 2021Review
- Network Pharmacology and Experimental Validation to Reveal the Pharmacological Mechanisms of Liuwei Dihuang Decoction Against Intervertebral Disc Degeneration.Drug design, development and therapy · 2021Article
- Inhibitory effects of astaxanthin on postovulatory porcine oocyte aging in vitro.Scientific reports · 2020Article
- Protocol for parallel proteomic and metabolomic analysis of mouse intervertebral disc tissues.JOR spine · 2020Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Approximately 40% of people under 30 and over 90% of people 55 or older suffer from moderate-to-severe levels of degenerative intervertebral disc (IVD) disease in their lumbar spines. Surgical treatments are sometimes effective; however, the treatment of back pain related to IVD degeneration is still a challenge; therefore, new treatments are necessary. Apoptosis may be important in IVD degeneration because suppressing cell apoptosis inside the IVD inhibits degeneration. Caspase-3, the primary effector of apoptosis, may be a key treatment target. We analyzed caspase-3's role in two different types of IVD degeneration using caspase-3 knockout (Casp-3 KO) mice. Casp-3 KO delayed IVD degeneration in the injury-induced model but accelerated it in the age-induced model. Our results suggest that this is due to different pathological mechanisms of these two types of IVD degeneration. Apoptosis was suppressed in the IVD cells of Casp-3 KO mice, but cellular senescence was enhanced. This would explain why the Casp-3 KO was effective against injury-induced, but not age-related, IVD degeneration. Our results suggest that short-term caspase-3 inhibition could be used to treat injury-induced IVD degeneration.
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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.