ReviewCell cycle (Georgetown, Tex.)2020
Telomeres: beacons of autocrine and paracrine DNA damage during skin aging.
Review in Cell cycle (Georgetown, Tex.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed.
- Telomere-associated non-malignant pulmonary diseases: Pathogenic mechanisms and therapeutic strategies.Acta pharmaceutica Sinica. B · 2026Review
- Royal jelly suppresses senescence-associated secretory phenotype in senescent human epidermal keratinocytes.Molecular biology reports · 2026Article
- GRWD1 as a Novel Signature and It Down Regulates IFN in Skin Aging.Cell biochemistry and function · 2026Article
- Cellular Senescence and SASP in Bladder Ageing: Mechanisms and Emerging Interventions.International journal of general medicine · 2026Review
- Inhibition and Rescue of Hyperglycemia-Induced Cellular Senescence by Mitochondrial Transfer from Enucleated Mesenchymal Stem Cell-Derived Microvesicles for Chronic Wound Healing.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Telomeres in skin aging.Biogerontology · 2025Review
- Senescence-like Phenotype After Chronic Exposure to Isoproterenol in Primary Quiescent Immune Cells.Biomolecules · 2024Article
- The brain-body energy conservation model of aging.Nature aging · 2024Review
- Tailoring biomaterials for skin anti-aging.Materials today. Bio · 2024Review
- Molecular mechanisms of aging and anti-aging strategies.Cell communication and signaling : CCS · 2024Review
- Selectively advantageous instability in biotic and pre-biotic systems and implications for evolution and aging.Frontiers in aging · 2024Review
- Mitochondrial dynamics and metabolism across skin cells: implications for skin homeostasis and aging.Frontiers in physiology · 2023Review
- Anti-aging effect of β-carotene through regulating the KAT7-P15 signaling axis, inflammation and oxidative stress process.Cellular & molecular biology letters · 2022Article
- How good is the evidence that cellular senescence causes skin ageing?Ageing research reviews · 2021Review
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.
Funding
Abstract
Cellular senescence is an irreversible cell cycle arrest, which can be triggered by a number of stressors, including telomere damage. Among many other phenotypic changes, senescence is accompanied by increased secretion of pro-inflammatory molecules, also known as the senescence-associated secretory phenotype (SASP). It is thought that accumulation of senescent cells contributes to age-associated tissue dysfunction partly by inducing senescence in neighboring cells through mechanisms involving SASP factors. Here, we will review evidence suggesting that telomeres can become dysfunctional irrespectively of shortening, and that this may be a mechanism-driving senescence in post-mitotic or slow dividing cells. Furthermore, we review recent evidence that supports that senescent melanocytes induce paracrine telomere damage during skin aging, which may be the mechanism responsible for propagation of senescent cells. We propose that telomeres are sensors of imbalances in the cellular milieu and act as beacons of stress, contributing to autocrine and paracrine senescence.
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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.