ArticleAging2011
Genome protective effect of metformin as revealed by reduced level of constitutive DNA damage signaling.
Article in Aging, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 52 citations in OpenAlex.
- Delaying Renal Aging: Metformin Holds Promise as a Potential Treatment.Aging and disease · 2024Review
- Review
- Benefits of Metformin in Attenuating the Hallmarks of Aging.Cell metabolism · 2020Review
- Senolytics and senostatics as adjuvant tumour therapy.EBioMedicine · 2019Review
- Cellular Senescence and the Kidney: Potential Therapeutic Targets and Tools.Frontiers in pharmacology · 2019Review
- Identifying the murine mammary cell target of metformin exposure.Communications biology · 2019Article
- New insight for metformin against bladder cancer.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2017Review
- Schedule-dependent increased efficiency of pemetrexed-ionizing radiation combination therapy elicits a differential DNA damage response in lung cancer cells.Cancer cell international · 2016Article
- Metformin for cancer and aging prevention: is it a time to make the long story short?Oncotarget · 2015Article
- Metformin ameliorates ionizing irradiation-induced long-term hematopoietic stem cell injury in mice.Free radical biology & medicine · 2015Article
- Cellular senescence: a hitchhiker's guide.Human cell · 2015Review
- Radiosensitization of pancreatic cancer cells by metformin through the AMPK pathway.Radiation research · 2014Article
- In search of antiaging modalities: evaluation of mTOR- and ROS/DNA damage-signaling by cytometry.Cytometry. Part A : the journal of the International Society for Analytical Cytology · 2014Review
- Metformin exhibits radiation countermeasures efficacy when used alone or in combination with sulfhydryl containing drugs.Radiation research · 2014Article
- Article
- Mitochondrial metabolic reprogramming induced by calorie restriction.Antioxidants & redox signaling · 2013Review
- Metformin improves healthspan and lifespan in mice.Nature communications · 2013 · on this mapArticle
- Hyper-mitogenic drive coexists with mitotic incompetence in senescent cells.Cell cycle (Georgetown, Tex.) · 2012Article
- Potential anti-aging agents suppress the level of constitutive mTOR- and DNA damage- signaling.Aging · 2012Article
- Advances in targeting signal transduction pathways.Oncotarget · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
We have shown before that constitutive DNA damage signaling represented by H2AX-Ser139 phosphorylation and ATM activation in untreated normal and tumor cells is a reporter of the persistent DNA replication stress induced by endogenous oxidants, the by-products of aerobic respiration. In the present study we observed that exposure of normal mitogenically stimulated lymphocytes or tumor cell lines A549, TK6 and A431 to metformin, the specific activator of 5'AMP-activated protein kinase (AMPK) and an inhibitor of mTOR signaling, resulted in attenuation of constitutive H2AX phosphorylation and ATM activation. The effects were metformin-concentration dependent and seen even at the pharmacologically pertinent 0.1 mM drug concentration. The data also show that intracellular levels of endogenous reactive oxidants able to oxidize 2',7'-dihydro-dichlorofluorescein diacetate was reduced in metformin-treated cells. Since persistent constitutive DNA replication stress, particularly when paralleled by mTOR signaling, is considered to be the major cause of aging, the present findings are consistent with the notion that metformin, by reducing both DNA replication stress and mTOR-signaling, slows down aging and/or cell senescence processes.
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.