ReviewDiabetologia2006
Chromosomal telomere attrition as a mechanism for the increased risk of epithelial cancers and senescent phenotypes in type 2 diabetes.
Review in Diabetologia, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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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.
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Who cites it
26 citing papers in PubMed, 59 citations in OpenAlex.
- Leukocyte telomere length and diabetes status, duration, and control: the 1999-2002 National Health and Nutrition Examination Survey.BMC endocrine disorders · 2015Trial
- Progress in the study of the role of C5a-induced tubular cell senescence in the progression of diabetic kidney disease.Annals of medicine · 2025Review
- Adenosine Monophosphate-Activated Protein Kinase Activation and Mammalian Target of Rapamycin Complex 1 Inhibition: A Mechanistic Rationale for Anti-Aging Therapy in Type 2 Diabetes.Journal of clinical medicine research · 2025Review
- Multistrain Probiotics and Telomere Length in Type 2 Diabetes: A 24-Week Randomized Controlled Trial.Life (Basel, Switzerland) · 2025Article
- Renal aging and its consequences: navigating the challenges of an aging population.Frontiers in pharmacology · 2025Review
- Review
- Evaluation of the effect of melatonin treatment on telomere length of the retinal pigment epithelium in streptozotocin-induced diabetic rat model.BMC ophthalmology · 2024Article
- Artesunate Alleviates Kidney Fibrosis in Type 1 Diabetes with Periodontitis Rats via Promoting Autophagy and Suppression of Inflammation.ACS omega · 2024Article
- Associations between type 2 diabetes mellitus and chronic liver diseases: evidence from a Mendelian randomization study in Europeans and East Asians.Frontiers in endocrinology · 2024Article
- Why and when should organisms elongate their telomeres? Elaborations on the 'excess resources elongation' and 'last resort elongation' hypotheses.Ecology and evolution · 2023Article
- Triglyceride-Glucose Index Correlate With Telomere Length in Healthy Adults From the National Health and Nutrition Examination Survey.Frontiers in endocrinology · 2022Article
- Cellular Senescence and Regulated Cell Death of Tubular Epithelial Cells in Diabetic Kidney Disease.Frontiers in endocrinology · 2022Review
- Role of Cellular Senescence in Type II Diabetes.Endocrinology · 2021Review
- Telomere Length Measurement by Molecular Combing.Frontiers in cell and developmental biology · 2020Article
- The Signaling of Cellular Senescence in Diabetic Nephropathy.Oxidative medicine and cellular longevity · 2019Review
- Comparison of telomere length measurement methods.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2018Review
- Global Gene Expression Profiling in Omental Adipose Tissue of Morbidly Obese Diabetic African Americans.Journal of endocrinology and metabolism · 2015Article
- Telomere length and pancreatic cancer: a case-control study.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2012Article
- STAT1 mediates cellular senescence induced by angiotensin II and H₂O₂ in human glomerular mesangial cells.Molecular and cellular biochemistry · 2012Article
- Indicators of "healthy aging" in older women (65-69 years of age). A data-mining approach based on prediction of long-term survival.BMC geriatrics · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Telomeres are the repeat DNA sequences at the end of chromosomes necessary for successful DNA replication and chromosomal integrity. Telomeres shorten at cell division at a rate determined by oxidative DNA damage, and cells are triggered into replicative senescence once telomeres shorten to a critical length. Telomere-related chromosomal maintenance also has a role in carcinogenesis. Type 2 diabetes is characterised by increased oxidative stress, increased oxidative DNA damage, senescent retinal and renal phenotypes, and an increased risk of epithelial malignancy. We suggest that increased oxidative DNA damage and telomere attrition in type 2 diabetes leads to: (1) carcinogenic telomere-dependent chromosomal non-reciprocal translocations, genomic instability, and the development of epithelial cancers; (2) senescent retinal and renal phenotypes (expressed as diabetic retinopathy and nephropathy); and (3) senescent vascular endothelial, monocyte-macrophage and vascular smooth muscle cells (expressed as endothelial dysfunction and accelerated atherogenesis). An adverse intrauterine environment leads to increased feto-placental oxidative stress and feto-placental oxidative DNA damage. We also suggest that intrauterine oxidative DNA damage and telomere shortening is another point at which increased oxidative stress could contribute to a pre-programmed increased risk of senescent phenotypes in adult offspring, characterised by type 2 diabetes and epithelial malignancy. These suggestions can be used to understand early glucose intolerance in the young children of type 1 diabetes pregnancies, poor cancer outcomes in type 2 diabetes, beta cell fatigue in type 2 diabetes and the absence of increased epithelial cancer risk in type 1 diabetes.
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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.