ArticleJournal of translational medicine2019
RIPK1 suppresses apoptosis mediated by TNF and caspase-3 in intervertebral discs.
Article in Journal of translational medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- Regulated cell death in musculoskeletal development, homeostasis, and diseases.Fundamental research · 2026Review
- Establishment of rabbit models of lumbar disc degeneration using three methods monitored via X-ray: a comparative study.Journal of orthopaedic surgery and research · 2025Article
- Apoptotic Pathway in Intervertebral Disc Degeneration: From Molecular Pathways to Clinical Interventions.Diagnostics (Basel, Switzerland) · 2025Review
- NOXA exacerbates endoplasmic-reticulum-stress-induced intervertebral disc degeneration by activating apoptosis and ECM degradation.Cell death discovery · 2025Article
- Significance of Necroptosis in Cartilage Degeneration.Biomolecules · 2024Review
- Inhibition of TRADD ameliorates chondrocyte necroptosis and osteoarthritis by blocking RIPK1-TAK1 pathway and restoring autophagy.Cell death discovery · 2023Article
- mRNA transcriptome profiling of human hepatocellular carcinoma cells HepG2 treated withWorld journal of hepatology · 2023Article
- Natural products can modulate inflammation in intervertebral disc degeneration.Frontiers in pharmacology · 2023Review
- Aging, cell senescence, the pathogenesis and targeted therapies of intervertebral disc degeneration.Frontiers in pharmacology · 2023Review
- Roles of receptor-interacting protein kinase 1 in SH-SY5Y cells with beta amyloid-induced neurotoxicity.Journal of cellular and molecular medicine · 2022Article
- Hydroxytyrosol Ameliorates Intervertebral Disc Degeneration and Neuropathic Pain by Reducing Oxidative Stress and Inflammation.Oxidative medicine and cellular longevity · 2022Article
- NF-κB signalling pathways in nucleus pulposus cell function and intervertebral disc degeneration.Cell proliferation · 2021Review
- Cartilage endplate stem cells inhibit intervertebral disc degeneration by releasing exosomes to nucleus pulposus cells to activate Akt/autophagy.Stem cells (Dayton, Ohio) · 2021Article
- TNFα in MS and Its Animal Models: Implications for Chronic Pain in the Disease.Frontiers in neurology · 2021Review
- Identification of Differentially Expressed circRNAs, miRNAs, and Genes in Patients Associated with Cartilaginous Endplate Degeneration.BioMed research international · 2021Article
- Overexpressed microRNA-494 represses RIPK1 to attenuate hippocampal neuron injury in epilepsy rats by inactivating the NF-κB signaling pathway.Cell cycle (Georgetown, Tex.) · 2020Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLow back pain has become a serious social and economic burden and the leading cause of disability worldwide. Among a variety of pathophysiological triggers, intervertebral disc (IVD) degeneration plays a primary underlying role in causing such pain. Specifically, multiple independent endplate changes have been implicated in the initiation and progression of IVD degeneration.
methodsIn this study, we built a signaling network comprising both well-characterized IVD pathology-associated proteins as well as some potentially correlated proteins that have been associated with one or more of the currently known pathology-associated proteins. We then screened for the potential IVD degeneration-associated proteins using patients' normal and degenerative endplate specimens. Short hairpin RNAs for receptor interacting serine/threonine kinase 1 (RIPK1) were constructed to examine the effects of RIPK1 knockdown in primary chondrocyte cells and in animal models of caudal vertebra intervertebral disc degeneration in vivo.
resultsRIPK1 was identified as a potential IVD degeneration-associated protein based on IVD pathology-associated signaling networks and the patients' degenerated endplate specimens. Construction of the short hairpin RNAs was successful, with short-term RIPK1 knockdown triggering inflammation in the primary chondrocytes, while long-term knockdown triggered apoptosis through cleavage of the caspase 3 pathway, down-regulated NF-κB and mitogen-activating protein kinase (MAPK)s cascades, and decreased cell survival and inflammation. Animal models of caudal vertebra intervertebral disc degeneration further demonstrated that apoptosis was induced by up-regulation of tumor necrosis factor (TNF) accompanied by down-regulation of NF-κB and MAPKs cascades that are dependent on caspase and RIPK1.
conclusionsThese results provide proof-of-concept for developing novel therapies to combat IVD degeneration through interfering with RIPK1-mediated apoptosis signaling pathways especially in patients with RIPK1 abnormality.
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