ArticleAge (Dordrecht, Netherlands)2012
Copper ability to induce premature senescence in human fibroblasts.
Article in Age (Dordrecht, Netherlands), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 60 citations in OpenAlex.
- Article
- Fisetin as a Blueprint for Senotherapeutic Agents - Elucidating Geroprotective and Senolytic Properties with Molecular Modeling.Chemistry (Weinheim an der Bergstrasse, Germany) · 2025Article
- Exploring Senolytic and Senomorphic Properties of Medicinal Plants for Anti-Aging Therapies.International journal of molecular sciences · 2024Article
- Early events marking lung fibroblast transition to profibrotic state in idiopathic pulmonary fibrosis.Respiratory research · 2023Article
- Among Gerontogens, Heavy Metals Are a Class of Their Own: A Review of the Evidence for Cellular Senescence.Brain sciences · 2023Review
- hsa-miR-508-5p as a New Potential Player in Intervertebral Disc Degeneration.International journal of molecular and cellular medicine · 2022Article
- The metabolic roots of senescence: mechanisms and opportunities for intervention.Nature metabolism · 2021Review
- Nuclear dynamics and stress responses in Alzheimer's disease.Molecular neurodegeneration · 2021Review
- Mangiferin, a naturally occurring polyphenol, mitigates oxidative stress induced premature senescence in human dermal fibroblast cells.Molecular biology reports · 2021Article
- Effect of antioxidants on the HAging · 2020Article
- The Mechanisms Underlying the Cytotoxic Effects of Copper Via Differentiated Embryonic Chondrocyte Gene 1.International journal of molecular sciences · 2019Article
- Article
- The Na/K-ATPase Oxidant Amplification Loop Regulates Aging.Scientific reports · 2018Article
- Effects of Melatonin and Its Underlying Mechanism on Ethanol-Stimulated Senescence and Osteoclastic Differentiation in Human Periodontal Ligament Cells and Cementoblasts.International journal of molecular sciences · 2018Article
- Copper accumulation in senescent cells: Interplay between copper transporters and impaired autophagy.Redox biology · 2018Article
- Happily (n)ever after: Aging in the context of oxidative stress, proteostasis loss and cellular senescence.Redox biology · 2017Review
- Mitochondrial DNA Hypomethylation Is a Biomarker Associated with Induced Senescence in Human Fetal Heart Mesenchymal Stem Cells.Stem cells international · 2017Article
- Resveratrol Attenuates Copper-Induced Senescence by Improving Cellular Proteostasis.Oxidative medicine and cellular longevity · 2017Article
- Silencing of the Menkes copper-transporting ATPase (Atp7a) gene increases cyclin D1 protein expression and impairs proliferation of rat intestinal epithelial (IEC-6) cells.Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS) · 2014Article
- Role of p38MAPK and oxidative stress in copper-induced senescence.Age (Dordrecht, Netherlands) · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human diploid fibroblasts (HDFs) exposed to subcytotoxic concentrations of oxidative or stressful agents, such as hydrogen peroxide, tert-butylhydroperoxide, or ethanol, undergo stress-induced premature senescence (SIPS). This condition is characterized by the appearance of replicative senescence biomarkers such as irreversible growth arrest, increase in senescence-associated β-galactosidase (SA β-gal) activity, altered cell morphology, and overexpression of several senescence-associated genes. Copper is an essential trace element known to accumulate with ageing and to be involved in the pathogenesis of some age-related disorders. Past studies using either yeast or human cellular models of ageing provided evidence in favor of the role of intracellular copper as a longevity modulator. In the present study, copper ability to cause the appearance of senescent features in HDFs was assessed. WI-38 fibroblasts exposed to a subcytotoxic concentration of copper sulfate presented inhibition of cell proliferation, cell enlargement, increased SA β-gal activity, and mRNA overexpression of several senescence-associated genes such as p21, apolipoprotein J (ApoJ), fibronectin, transforming growth factor β-1 (TGF β1), insulin growth factor binding protein 3, and heme oxygenase 1. Western blotting results confirmed enhanced intracellular p21, ApoJ, and TGF β1 in copper-treated cells. Thus, similar to other SIPS-inducing agents, HDF exposure to subcytotoxic concentration of copper results in premature senescence. Further studies will unravel molecular mechanisms and the biological meaning of copper-associated senescence and lead to a better understanding of copper-related disorder establishment and progression.
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.