ArticleScientific reports2021
Cellular senescence promotes endothelial activation through epigenetic alteration, and consequently accelerates atherosclerosis.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 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
52 citing papers in PubMed, 69 citations in OpenAlex.
- Endothelial Matrin-3 Limits Cellular Senescence and Lipid Dysregulation to Protect Against Murine Atherosclerosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Cellular senescence: six decades of discovery and reinvention.The EMBO journal · 2026Review
- The role of senescence in kidney ageing, injury and fibrosis.Nature reviews. Nephrology · 2026Review
- Terpenoids as modulators of autophagy-senescence crosstalk in lung cancer.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2026Review
- Inflammaging and cytokine-driven cardiovascular senescence in age-related myocardial infarction: mechanisms, biomarkers, and precision immunotherapy strategies.Biogerontology · 2026Review
- Inflammation in atherosclerosis: Drivers, mechanisms and therapies.Acta pharmaceutica Sinica. B · 2026Review
- One-carbon metabolism and cardiovascular disease: Molecular mechanisms, genetic influences, and epigenetic regulation.Biochemistry and biophysics reports · 2026Review
- Senolytic Treatment With Fisetin Reverses Age-Related Endothelial Dysfunction Partially Mediated by SASP Factor CXCL12.Aging cell · 2026Article
- Mitochondrial dysfunction in endothelial senescence: implications for vascular remodeling and therapeutic strategies.Archives of pharmacal research · 2026Review
- The Role of Cellular Senescence and SASP in the Pathogenesis of Atherosclerosis and the Therapeutic Potential of Senolytic Strategies in Cardiovascular Diseases.Biomedicines · 2026Review
- Virus-induced endothelial senescence as a cause and driving factor for ME/CFS and long COVID: mediated by a dysfunctional immune system.Cell death & disease · 2026Review
- Replicative and stress-induced premature senescence distinctively affect the endothelial anticoagulation capacity.PloS one · 2026Article
- Cellular Senescence, Inflammaging and Cardiovascular Disease.Immunological reviews · 2026Review
- Cellular and Molecular Mechanisms of Vascular Endothelial Injury Induced by Cigarette Smoke and Cigarette Smoke Extract in Atherosclerosis.Journal of inflammation research · 2026Review
- Endothelial barrier and sepsis: mechanisms and potential therapeutic strategies.Military Medical Research · 2026Review
- The role of cellular senescence in cardiovascular disease.Cell death discovery · 2025Review
- Quercetin ameliorates ox-LDL-induced cellular senescence of aortic endothelial cells and macrophages by p16/p21, p53/SERPINE1, and AMPK/mTOR pathways.European journal of medical research · 2025Article
- Review
- Is Senolytic Therapy in Cardiovascular Diseases Ready for Translation to Clinics?Biomolecules · 2025Review
- The role of senescence-related genes in major depressive disorder: insights from machine learning and single cell analysis.BMC psychiatry · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Senescent vascular cells are detected in atherosclerotic lesion, and its involvement in the development of atherosclerosis has been revealed; however, whether and the mechanism by which endothelial cell (EC) senescence is causally implicated in atherosclerosis remains unclear. We here investigate a role of EC senescence in atherosclerosis by utilizing EC-specific progeroid mice that overexpress the dominant negative form of telomeric repeat-binding factor 2 under the control of the Tie2 or vascular endothelial cadherin promoter. EC-specific progeria accelerated atherosclerosis in mice with target deletion of ApoE. Mechanistically, senescent ECs were markedly sensitive for inflammation-mediated VCAM-1 induction, leading to enhanced monocyte adhesion. Inhibition of NF-κB signaling abolished the enhanced inflammatory responses in senescent ECs, while NF-κB nuclear translocation in response to TNF-α were similar between young and senescent ECs. We found a higher association of VCAM-1 gene with active histone H3 trimethylated on lysine 4, leading to increased NF-κB accessibility in senescent ECs. Our data revealed that EC cellular senescence causes endothelial hyper-inflammability through epigenetic alteration, which consequently accelerates atherosclerosis. Therefore, EC senescence is a promising therapeutic target for the prevention and/or treatment of atherosclerotic disease in elderly population.
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.