ReviewMicrocirculation (New York, N.Y. : 1994)2019
The role of senescence, telomere dysfunction and shelterin in vascular aging.
Review in Microcirculation (New York, N.Y. : 1994), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.
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
44 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.
- A Systematic Review of the Association Between Muscular Fitness and Telomere Length Across the Adult Lifespan.Frontiers in physiology · 2021Pooled it
- Aging and DNA damage are associated with the development of endothelial cell clonal expansion.American journal of physiology. Heart and circulatory physiology · 2026Article
- Direct in vivo reprogramming to relieve tissue ischemia via induced vasculogenesis.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- MitoQ reduces senescence burden in doxorubicin-treated endothelial cells by reducing mitochondrial ROS and DNA damage.American journal of physiology. Heart and circulatory physiology · 2025Article
- Cerebrovascular protective functions of amyloid precursor protein: Progress and therapeutic prospects.Pharmacology & therapeutics · 2025Review
- The aging male: impact of aging on male reproduction.Biogerontology · 2025Review
- Review of the Role of TRAF7 in Brain Endothelial Integrity and Cerebrovascular Aging.Life (Basel, Switzerland) · 2025Review
- Deletion of PTHrP nuclear localization sequence and carboxyl terminus leads to lung dysplasia.Scientific reports · 2025Article
- Oxidized Low-Density Lipoprotein and Its Role in Immunometabolism.International journal of molecular sciences · 2024Review
- α-Terpineol Induces Shelterin Components TRF1 and TRF2 to Mitigate Senescence and Telomere Integrity Loss via A Telomerase-Independent Pathway.Antioxidants (Basel, Switzerland) · 2024Article
- Review
- Associations of measured and genetically predicted leukocyte telomere length with vascular phenotypes: a population-based study.GeroScience · 2024Article
- Leukocyte telomere length and sarcopenia-related traits: A bidirectional Mendelian randomization study.PloS one · 2024Article
- Geroscience and pathology: a new frontier in understanding age-related diseases.Pathology oncology research : POR · 2024Review
- New Dawn for Atherosclerosis: Vascular Endothelial Cell Senescence and Death.International journal of molecular sciences · 2023Review
- Non-Excitatory Amino Acids, Melatonin, and Free Radicals: Examining the Role in Stroke and Aging.Antioxidants (Basel, Switzerland) · 2023Review
- Article
- Endothelial cell telomere dysfunction induces senescence and results in vascular and metabolic impairments.Aging cell · 2023Article
- Mechanisms and consequences of endothelial cell senescence.Nature reviews. Cardiology · 2023Review
- Senolytics Reduce Endothelial Cell DNA Damage and Telomere Dysfunction Despite Reductions in Telomere Length.Aging biology · 2023Article
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 1 institution in 2 countries.
Funding
Abstract
In the United States and other westernized nations, CVDs are the leading cause of death in adults over 65 years of age. Large artery stiffness and endothelial dysfunction are increased with age and age-associated arterial dysfunction is an important antecedent of CVDs. One age-associated change that may contribute to vascular dysfunction and CVD risk is an increase in the number of resident senescent cells in the vasculature. Senescent cells display a pro-oxidant, pro-inflammatory phenotype known as the SASP. However, the mechanisms that drive the SASP and the vascular aging phenotype remain elusive. A putative mechanism is the involvement of oxidative stress and inflammation in telomere function. Telomeres are the end caps of chromosomes which are maintained by a six-protein complex known as shelterin. Disruption of shelterin can uncap telomeres and induce cellular senescence. Accordingly, in this review, we propose that oxidative stress and inflammation disrupt shelterin in vascular cells, driving telomere dysfunction and that this mechanism may be responsible for the induction of SASP. The proposed mechanisms may represent some of the initial changes that lead to vascular dysfunction in advanced age.
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.