ArticleAging2018
Rapamycin prevents the intervertebral disc degeneration via inhibiting differentiation and senescence of annulus fibrosus cells.
Article in Aging, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
32 citing papers in PubMed, 42 citations in OpenAlex.
- Closing the gap in aging science: unlocking the potential of nanoparticles in senescence therapy.Biogerontology · 2026Review
- The role and potential therapeutic intervention of cellular senescence in intervertebral disc degeneration.Genes & diseases · 2026Review
- Autophagy activation alleviates annulus fibrosus degeneration via the miR-2355-5p/mTOR pathway.Journal of orthopaedic surgery and research · 2025Article
- Tissue engineering strategies for treating intervertebral disc degeneration.Frontiers in bioengineering and biotechnology · 2025Review
- Identification and Experimental Verification of Potential Immune Cell-Associated Gene Biomarkers in Human Intervertebral Disc Degeneration.Journal of pain research · 2025Article
- Modulation of fracture healing by senescence-associated secretory phenotype (SASP): a narrative review of the current literature.European journal of medical research · 2024Review
- From drugs to biomaterials: a review of emerging therapeutic strategies for intervertebral disc inflammation.Frontiers in cellular and infection microbiology · 2024Review
- Intervertebral Disc Progenitors: Lessons Learned from Single-Cell RNA Sequencing and the Role in Intervertebral Disc Regeneration.Bioengineering (Basel, Switzerland) · 2023Article
- Intervertebral disc cell fate during aging and degeneration: apoptosis, senescence, and autophagy.North American Spine Society journal · 2023Article
- Cellular Senescence in Intervertebral Disc Aging and Degeneration: Molecular Mechanisms and Potential Therapeutic Opportunities.Biomolecules · 2023Review
- Article
- Inflammation produced by senescent osteocytes mediates age-related bone loss.Frontiers in immunology · 2023Article
- Emerging role and therapeutic implication of mTOR signalling in intervertebral disc degeneration.Cell proliferation · 2023Review
- Barriers to mesenchymal stromal cells for low back pain.World journal of stem cells · 2022Article
- Cyanidin attenuates the apoptosis of rat nucleus pulposus cells and the degeneration of intervertebral disc via the JAK2/STAT3 signal pathwayPharmaceutical biology · 2022Article
- Cell senescence, rapamycin and hyperfunction theory of aging.Cell cycle (Georgetown, Tex.) · 2022Review
- Elimination of Senescent Cells by Senolytics Facilitates Bony Endplate Microvessel Formation and Mitigates Disc Degeneration in Aged Mice.Frontiers in cell and developmental biology · 2022Article
- The Role of Senescence-Associated Secretory Phenotype in Bone Loss.Frontiers in cell and developmental biology · 2022Review
- Senolytics: Eliminating Senescent Cells and Alleviating Intervertebral Disc Degeneration.Frontiers in bioengineering and biotechnology · 2022Review
- Cell sources proposed for nucleus pulposus regeneration.JOR spine · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The effects of bleomycin and rapamycin on cellular senescence and differentiation of rabbit annulus fibrosus stem cells (AFSCs) were investigated using a cell culture model. The results showed that bleomycin induced cellular senescence in AFSCs as evidenced by senescence-associated secretory phenotype. The morphology of AFSCs was changed from cobblestone-like cells to pancake-like cells. The senescence-associated β-galactosidase activity, the protein expression of P16 and P21, and inflammatory-related marker gene levels IL-1β, IL-6, and TNF-α were increased in bleomycin-treated AFSCs in a dose-dependent manner. Rapamycin treatment decreased the gene expression of MMP-3, MMP-13, IL-1β, IL-6, TNF-α, and protein levels of P16 and P21 in bleomycin-treated AFSCs. Furthermore, neither bleomycin nor rapamycin changed the ribosomal S6 protein level in AFSCs. However, the phosphorylation of the ribosomal S6 protein was increased in bleomycin-treated AFSCs and decreased in rapamycin-treated AFSCs. AFSCs differentiated into adipocytes, osteocytes, and chondrocytes when they were cultured with respective differentiation media. Rapamycin inhibited multi-differentiation potential of AFSCs in a concentration-dependent manner. Our findings demonstrated that mammalian target of rapamycin (mTOR) signaling affects cellular senescence, catabolic and inflammatory responses, and multi-differentiation potential, suggesting that potential treatment value of rapamycin for disc degenerative diseases, especially lower back pain.
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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.