In cell senescence, cultured cells cease proliferating and acquire aberrant gene expression patterns. MicroRNAs (miRNAs) modulate gene expression through translational repression or mRNA degradation and have been implicated in senescence. We used deep sequencing to carry out a comprehensive survey of miRNA expression and involvement in cell senescence. Informatic analysis of small RNA sequence datasets from young and senescent IMR90 human fibroblasts identifies many miRNAs that are regulated (either up or down) with cell senescence. Comparison with mRNA expression profiles reveals potential mRNA targets of these senescence-regulated miRNAs. The target mRNAs are enriched for genes involved in biological processes associated with cell senescence. This result greatly extends existing information on the role of miRNAs in cell senescence and is consistent with miRNAs having a causal role in the process.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3102725 | PMC |
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0020509 | PLOS |
Cell Biosci
January 2025
School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong S.A.R., China.
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Sorbonne Université, CNRS, Laboratory of Computational and Quantitative Biology, LCQB, Paris, France.
Telomere shortening ultimately causes replicative senescence. However, identifying the mechanisms driving replicative senescence in cell populations is challenging due to the heterogeneity of telomere lengths and the asynchrony of senescence onset. Here, we present a mathematical model of telomere shortening and replicative senescence in Saccharomyces cerevisiae which is quantitatively calibrated and validated using data of telomerase-deficient single cells.
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January 2025
Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA.
Alzheimer's disease (AD) is the most common type of dementia and one of the leading causes of death in elderly patients. The number of patients with AD in the United States is projected to double by 2060. Thus, understanding modifiable risk factors for AD is an urgent public health priority.
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January 2025
College of Life Science, Yangtze University, Jingzhou 434025, China. Electronic address:
Cellular senescence precipitates a decline in physiological activities and metabolic functions, often accompanied by heightened inflammatory responses, diminished immune function, and impaired tissue and organ performance. Despite extensive research, the mechanisms underpinning cellular senescence remain incompletely elucidated. Emerging evidence implicates circadian rhythm and hypoxia as pivotal factors in cellular senescence.
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January 2025
Gale and Ira Drukier Institute for Children's Health, Weill Cornell Medicine, New York, NY 10065, United States; Department of Pediatrics, Weill Cornell Medicine, New York, NY 10065, United States; Immunology and Microbial Pathogenesis Program, Weill Cornell Graduate School, New York, NY 10065, United States. Electronic address:
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