ArticleCell death & disease2018
Ubiquitin C decrement plays a pivotal role in replicative senescence of bone marrow mesenchymal stromal cells.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 23 citations in OpenAlex.
- Long noncoding RNA SRRM2-AS1 mediates coronary artery damage in Kawasaki disease by promoting endothelial-to-mesenchymal transition.Clinical and experimental medicine · 2026Article
- A Comprehensive Multiomics Signature of Doxorubicin-Induced Cellular Senescence in the Postmenopausal Human Ovary.Aging cell · 2025Article
- Tracing genomic instability in induced mesenchymal stromal cell manufacture: an integration-free transfection approach.Experimental & molecular medicine · 2025Article
- The syntaxin-binding protein STXBP5 regulates progerin expression.Scientific reports · 2024Article
- Influence of the Bone Marrow Microenvironment on Hematopoietic Stem Cell Behavior Post-Allogeneic Transplantation: Development of Clonal Hematopoiesis and Telomere Dynamics.International journal of molecular sciences · 2024Article
- Young small extracellular vesicles rejuvenate replicative senescence by remodeling Drp1 translocation-mediated mitochondrial dynamics.Journal of nanobiotechnology · 2024Article
- YAP Inhibition Alleviates Simulated Microgravity-Induced Mesenchymal Stem Cell Senescence via Targeting Mitochondrial Dysfunction.Antioxidants (Basel, Switzerland) · 2023Article
- Ginsenoside Rg2 Promotes the Proliferation and Stemness Maintenance of Porcine Mesenchymal Stem Cells through Autophagy Induction.Foods (Basel, Switzerland) · 2023Article
- UBC Mediated by SEPT6 Inhibited the Progression of Prostate Cancer.Mediators of inflammation · 2021Article
- To Breathe or Not to Breathe: The Role of Oxygen in Bone Marrow-Derived Mesenchymal Stromal Cell Senescence.Stem cells international · 2021Review
- Adult mesenchymal stem cell ageing interplays with depressed mitochondrial Ndufs6.Cell death & disease · 2020Article
- Article
- Common and different alterations of bone marrow mesenchymal stromal cells in myelodysplastic syndrome and multiple myeloma.Cell proliferation · 2020Article
- Transcriptome signature of cellular senescence.Nucleic acids research · 2019Article
- FGF21 Mediates Mesenchymal Stem Cell Senescence via Regulation of Mitochondrial Dynamics.Oxidative medicine and cellular longevity · 2019Article
- Effects of senescent secretory phenotype acquisition on human retinal pigment epithelial stem cells.Aging · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human bone marrow-mesenchymal stromal cells (hBM-MSCs) undergo cellular senescence during in vitro culture. In this study, we defined this replicative senescence as impaired proliferation, deterioration in representative cell characteristics, accumulated DNA damage, and decreased telomere length and telomerase activity with or without genomic abnormalities. The UBC gene expression gradually decreased during passaging along with the reduction in series of molecules including hub genes; CDK1, CCNA2, MCM10, E2F1, BRCA1, HIST1H1A and HIST1H3B. UBC knockdown in hBM-MSCs induced impaired proliferation in dose-dependent manner and showed replicative senescence-like phenomenon. Gene expression changes after UBC knockdown were similar to late passage hBM-MSCs. Additionally, UBC overexpession improved the proliferation activity of hBM-MSCs accompanied by increased expression of the hub genes. Consequently, UBC worked in higher-order through regulation of the hub genes controlling cell cycle and proliferation. These results indicate that the decrement of UBC expression plays a pivotal role in replicative senescence of hBM-MSCs.
Indexed as
Identifiers
What OpenQuestion holds
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.