ArticleFrontiers in cell and developmental biology2020
Inhibiting Heat Shock Protein 90 Protects Nucleus Pulposus-Derived Stem/Progenitor Cells From Compression-Induced Necroptosis and Apoptosis.
Article in Frontiers in cell and developmental biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 43 citations in OpenAlex.
- Proteostasis Dysfunction and Heat Shock Protein Networks in Intervertebral Disc Degeneration: Molecular Mechanisms and Therapeutic Opportunities.Current issues in molecular biology · 2026Review
- Biomechanical effects of different intervertebral height reconstructions on the intermediate segment in skip-level ACDF for discontinuous cervical spondylosis: a finite element analysis.BMC musculoskeletal disorders · 2026Article
- Intervertebral disc progenitor cells: roles in regeneration and disease.Stem cell research & therapy · 2026Review
- USP39 inhibits MLKL phosphorylation and deubiquitination to suppress necroptosis of nucleus pulposus cells and attenuate intervertebral disc degeneration.Journal of orthopaedic translation · 2026Article
- Natural products targeting programmed cell death: a novel therapeutic strategy for intervertebral disc degeneration.International journal of surgery (London, England) · 2026Review
- Regulated cell death in musculoskeletal development, homeostasis, and diseases.Fundamental research · 2026Review
- The role of nucleus pulposus progenitor cells in intervertebral disc degeneration and regeneration.Journal of orthopaedic surgery and research · 2025Review
- In Vitro Release and In Vivo Study of Recombinant TGF-β and EGCG from Dual Self-Cross-Linked Alginate-Di-AldehydeGels (Basel, Switzerland) · 2025Article
- Exploring the critical role of PANoptosis in the pathogenesis of intervertebral disc degeneration: mechanisms and potential therapeutic targets.Frontiers in cell and developmental biology · 2025Review
- Investigating the characteristics of mild intervertebral disc degeneration at various age stages using single-cell genomics.Frontiers in cell and developmental biology · 2024Article
- Article
- HSP90B1 regulates autophagyPeerJ · 2024Article
- Review
- Systematic pharmacology-based strategy to investigate the mechanism of beta-sitosterol for the treatment of rheumarthritis.Frontiers in genetics · 2024Article
- Bioinformatics Analysis of Biomarkers and Therapeutic Targets Related to Necroptosis in Intervertebral Disc Degeneration.BioMed research international · 2024Article
- HSPA8 acts as an amyloidase to suppress necroptosis by inhibiting and reversing functional amyloid formation.Cell research · 2023Article
- Role of Necroptosis in Intervertebral Disc Degeneration.International journal of molecular sciences · 2023Review
- Role of heat shock protein 90 as an antiviral target for swine enteric coronaviruses.Virus research · 2023Article
- HSP90 mediates the connection of multiple programmed cell death in diseases.Cell death & disease · 2022Review
- Regulated cell death: Implications for intervertebral disc degeneration and therapy.Journal of orthopaedic translation · 2022Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nucleus pulposus-derived stem/progenitor cells (NPSCs) provide novel prospects for the regeneration of degenerated intervertebral disc (IVD). Nevertheless, with aging and degeneration of IVD, the frequency of NPSCs markedly decreases. Excessive cell death could be the main reason for declined frequency of NPSCs, however, the exact mechanisms remain elusive. Thus, the present study was undertaken to explore the mechanisms of compression-induced NPSCs death, and the effects of heat shock protein 90 (HSP90) on NPSCs survival. Here, we found that compression could trigger receptor-interacting protein kinase 1 (RIPK1)/receptor-interacting protein kinase 3 (RIPK3)/mixed lineage kinase domain-like protein (MLKL)-mediated necroptosis of NPSCs. Furthermore, we found that elevated expression of HSP90 was involved in compression-induced NPSCs death, and inhibiting HSP90 could dramatically attenuate compression-induced necroptosis of NPSCs via regulating the expression and activity of RIPK1/RIPK3/MLKL, and alleviating the mitochondrial dysfunction (mitochondrial membrane potential loss and ATP depletion) and oxidative stress [production of mitochondrial reactive oxygen species (ROS), cellular total ROS and malondialdehyde, and downregulation of superoxide dismutase 2]. Besides necroptosis, compression-induced apoptosis of NPSCs was also attenuated by HSP90 inhibition. In addition, we found that enhanced expression of HSP70 contributed to the cytoprotective effects of inhibiting HSP90. More encouragingly, our results demonstrated that inhibiting HSP90 could also mitigate the exhaustion of NPSCs
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