ArticleFrontiers in neuroscience2021
Cellular Senescence Triggers Altered Circadian Clocks With a Prolonged Period and Delayed Phases.
Article in Frontiers in neuroscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- Circadian synchronization between diet and gut microbiota in modulating host's health.Gut microbes · 2026Review
- Circadian disruption and cellular senescence: emerging perspectives in periodontitis.Odontology · 2026Review
- Cellular circadian period and its deviation associate with Alzheimer's pathology and brain aging in cognitively impaired older adults.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Senescence-circadian interplay stratifies patient prognosis and reveals immune remodeling heterogeneity in colorectal cancer.Frontiers in immunology · 2026Article
- Sleep Disorders in Neurodegenerative Diseases with Dementia: A Comprehensive Review.Journal of clinical medicine · 2025Review
- Urolithin A Modulates PER2 Degradation via SIRT1 and Enhances the Amplitude of Circadian Clocks in Human Senescent Cells.Nutrients · 2024Article
- Stress Hormones: Unveiling the Role in Accelerated Cellular Senescence.Aging and disease · 2024Review
- A coupled model between circadian, cell-cycle, and redox rhythms reveals their regulation of oxidative stress.Scientific reports · 2024Article
- Vutiglabridin Alleviates Cellular Senescence with Metabolic Regulation and Circadian Clock in Human Dermal Fibroblasts.Antioxidants (Basel, Switzerland) · 2024Article
- Boltzmann's Theorem Revisited: Inaccurate Time-to-Action Clocks in Affective Disorders.Current neuropharmacology · 2024Review
- Targeting accelerated pulmonary ageing to treat chronic obstructive pulmonary disease-induced neuropathological comorbidities.British journal of pharmacology · 2024Review
- BMAL1 modulates senescence programming via AP-1.Aging · 2023Article
- Life's Essential 8: Optimizing Health in Older Adults.JACC. Advances · 2023Article
- Circadian Oscillations in Skin and Their Interconnection with the Cycle of Life.International journal of molecular sciences · 2023Review
- Emerging Insight Into the Role of Circadian Clock Gene BMAL1 in Cellular Senescence.Frontiers in endocrinology · 2022Review
- Telomere Shortening and Its Association with Cell Dysfunction in Lung Diseases.International journal of molecular sciences · 2021Review
- Attenuated SIRT1 Activity Leads to PER2 Cytoplasmic Localization and Dampens the Amplitude ofFrontiers in neuroscience · 2021Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Senescent cells, which show the permanent growth arrest in response to various forms of stress, accumulate in the body with the progression of age, and are associated with aging and age-associated diseases. Although the senescent cells are growth arrested, they still demonstrate high metabolic rate and altered gene expressions, indicating that senescent cells are still active. We recently showed that the circadian clock properties, namely phase and period of the cells, are altered with the establishment of replicative senescence. However, whether cellular senescence triggers the alteration of circadian clock properties in the cells is still unknown. In this study we show that the oxidative stress-induced premature senescence induces the alterations of the circadian clock, similar to the phenotypes of the replicative senescent cells. We found that the oxidative stress-induced premature senescent cells display the prolonged period and delayed phases. In addition, the magnitude of these changes intensified over time, indicating that cellular senescence changes the circadian clock properties. Our current results corroborate with our previous findings and further confirm that cellular senescence induces altered circadian clock properties, irrespective of the replicative senescence or the stress-induced premature senescence.
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