ArticlePloS one2015
A Model for p38MAPK-Induced Astrocyte Senescence.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 40 citations in OpenAlex.
- Sex Differences in Astrocyte Activity.Cells · 2024Review
- Glaucoma: from pathogenic mechanisms to retinal glial cell response to damage.Frontiers in cellular neuroscience · 2024Review
- Blood-brain barrier dysfunction promotes astrocyte senescence through albumin-induced TGFβ signaling activation.Aging cell · 2023Article
- Molecular Mechanisms of Neuroinflammation in Aging and Alzheimer's Disease Progression.International journal of molecular sciences · 2023Review
- Synergistic effects of complex drug combinations in colorectal cancer cells predicted by logical modelling.Frontiers in systems biology · 2023Article
- Δ133p53α Protects Human Astrocytes from Amyloid-beta Induced Senescence and Neurotoxicity.Neuroscience · 2022Article
- Blood-Brain Barrier Dysfunction and Astrocyte Senescence as Reciprocal Drivers of Neuropathology in Aging.International journal of molecular sciences · 2022Review
- Abnormal expression of cortical cell cycle regulators underlying anxiety and depressive-like behavior in mice exposed to chronic stress.Frontiers in cellular neuroscience · 2022Article
- YAP prevents premature senescence of astrocytes and cognitive decline of Alzheimer's disease through regulating CDK6 signaling.Aging cell · 2021Article
- Mild cognitive impairment and major depressive disorder are associated with molecular senescence abnormalities in older adults.Alzheimer's & dementia (New York, N. Y.) · 2021Article
- Systems biology approach suggests new miRNAs as phenotypic stability factors in the epithelial-mesenchymal transition.Journal of the Royal Society, Interface · 2020Article
- Advanced Age Increases Immunosuppression in the Brain and Decreases Immunotherapeutic Efficacy in Subjects with Glioblastoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2020Article
- Regulation of senescence traits by MAPKs.GeroScience · 2020Review
- Integrative data modeling from lung and lymphatic cancer predicts functional roles for miR-34a and miR-16 in cell fate regulation.Scientific reports · 2020Article
- Expression of p16 and p21 in the frontal association cortex of ALS/MND brains suggests neuronal cell cycle dysregulation and astrocyte senescence in early stages of the disease.Neuropathology and applied neurobiology · 2020Article
- Article
- Astrocyte Senescence and Alzheimer's Disease: A Review.Frontiers in aging neuroscience · 2020Review
- Screening Method for Identifying Toxicants Capable of Inducing Astrocyte Senescence.Toxicological sciences : an official journal of the Society of Toxicology · 2018Article
- Early Life Stress and Epigenetics in Late-onset Alzheimer's Dementia: A Systematic Review.Current genomics · 2018Review
- Ageing, Cellular Senescence and Neurodegenerative Disease.International journal of molecular sciences · 2018Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Experimental evidence indicates that aging leads to accumulation of senescent cells in tissues and they develop a secretory phenotype (also known as SASP, for senescence-associated secretory phenotype) that can contribute to chronic inflammation and diseases. Recent results have showed that markers of senescence in astrocytes from aged brains are increased in brains with Alzheimer's disease. These studies strongly involved the stress kinase p38MAPK in the regulation of the secretory phenotype of astrocytes, yet the molecular mechanisms underlying the onset of senescence and SASP activation remain unclear. In this work, we propose a discrete logical model for astrocyte senescence determined by the level of DNA damage (reparable or irreparable DNA strand breaks) where the kinase p38MAPK plays a central role in the regulation of senescence and SASP. The model produces four alternative stable states: proliferation, transient cycle arrest, apoptosis and senescence (and SASP) computed from its inputs representing DNA damages. Perturbations of the model were performed through gene gain or loss of functions and compared with results concerning cultures of normal and mutant astrocytes showing agreement in most cases. Moreover, the model allows some predictions that remain to be tested experimentally.
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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.