ArticleAging cell2024
Endothelial-specific telomerase inactivation causes telomere-independent cell senescence and multi-organ dysfunction characteristic of aging.
Article in Aging cell, 2024. 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
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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
21 citing papers in PubMed, 26 citations in OpenAlex.
- Mechanisms and integrative machine learning approaches to blood-brain barrier biomarker profiling for personalized ischemic stroke management.Physiological reports · 2026Review
- The aging paradox of Cushing's syndrome: Stress without clear senescence?Journal of neuroendocrinology · 2026Review
- Construction of TERT Monoallelic Knockout and TERT Overexpression of Porcine Cell Lines and Study of the Cellular Biological Characteristics.Animals : an open access journal from MDPI · 2026Article
- Glucose and Lipid Metabolic Mechanisms in Vascular Aging and Related Therapeutic Strategies.Reviews in cardiovascular medicine · 2026Review
- Telomerase Knockout in Myeloid Cells Predisposes Mice to Foam Cell Formation, Dyslipidemia, Lung Fibrosis, and Cardiac Dysfunction.Aging cell · 2026Article
- Article
- Microvascular Health as a Key Determinant of Organismal Aging.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Endothelial TERT drives microvascular phenotype associated with coronary artery disease.American journal of physiology. Heart and circulatory physiology · 2025Article
- Article
- Role of Nutritional Elements in Skin Homeostasis: A Review.Biomolecules · 2025Review
- Review
- Telomeres in skin aging.Biogerontology · 2025Review
- Redox regulation: mechanisms, biology and therapeutic targets in diseases.Signal transduction and targeted therapy · 2025Review
- Article
- Exploring the Link Between Telomeres and Mitochondria: Mechanisms and Implications in Different Cell Types.International journal of molecular sciences · 2025Review
- UTX/Top2β axis mediated spinal cord microvascular endothelial cells senescence exacerbates spinal cord injury.PloS one · 2025Article
- Mechanisms of cellular senescence-induced vascular aging: evidence of senotherapeutic strategies.The journal of cardiovascular aging · 2025Article
- FOXO4-DRI regulates endothelial cell senescence via the P53 signaling pathway.Frontiers in bioengineering and biotechnology · 2025Article
- Review
- Mechanisms and metabolic consequences of adipocyte progenitor replicative senescence.Immunometabolism (Cobham, Surrey) · 2024Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
It has remained unclear how aging of endothelial cells (EC) contributes to pathophysiology of individual organs. Cell senescence results in part from inactivation of telomerase (TERT). Here, we analyzed mice with Tert knockout specifically in EC. Tert loss in EC induced transcriptional changes indicative of senescence and tissue hypoxia in EC and in other cells. We demonstrate that EC-Tert-KO mice have leaky blood vessels. The blood-brain barrier of EC-Tert-KO mice is compromised, and their cognitive function is impaired. EC-Tert-KO mice display reduced muscle endurance and decreased expression of enzymes responsible for oxidative metabolism. Our data indicate that Tert-KO EC have reduced mitochondrial content and function, which results in increased dependence on glycolysis. Consistent with this, EC-Tert-KO mice have metabolism changes indicative of increased glucose utilization. In EC-Tert-KO mice, expedited telomere attrition is observed for EC of adipose tissue (AT), while brain and skeletal muscle EC have normal telomere length but still display features of senescence. Our data indicate that the loss of Tert causes EC senescence in part through a telomere length-independent mechanism undermining mitochondrial function. We conclude that EC-Tert-KO mice is a model of expedited vascular senescence recapitulating the hallmarks aging, which can be useful for developing revitalization therapies.
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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 Socratic graph.