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Amelioration of premature aging in Werner syndrome stem cells by targeting SHIP/AKT pathway.
Cell Biosci
January 2025
School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong S.A.R., China.
Background: Pathogenic or null mutations in WRN helicase is a cause of premature aging disease Werner syndrome (WS). WRN is known to protect somatic cells including adult stem cells from premature senescence. Loss of WRN in mesenchymal stem cells (MSCs) not only drives the cells to premature senescence but also significantly impairs the function of the stem cells in tissue repair or regeneration.
View Article and Find Full Text PDFMathematical model linking telomeres to senescence in Saccharomyces cerevisiae reveals cell lineage versus population dynamics.
Nat Commun
January 2025
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.
View Article and Find Full Text PDFThe biological intersection between chemotherapy-related cognitive impairment and Alzheimer's disease.
Am J Pathol
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.
View Article and Find Full Text PDFCircadian Rhythm, Hypoxia, and Cellular Senescence: From Molecular Mechanisms to Targeted Strategies.
Eur J Pharmacol
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.
View Article and Find Full Text PDFSynthesis of Arginase Inhibitors: An Overview.
Pharmaceutics
January 2025
Department of Pharmacy, "Federico II" University of Naples, 80131 Naples, Italy.
Arginase (ARG) is a binuclear manganese-containing metalloenzyme that can convert L-arginine to L-ornithine and urea and plays a key role in the urea cycle. It also mediates different cellular functions and processes such as proliferation, senescence, apoptosis, autophagy, and inflammatory responses in various cell types. In mammals, there are two isoenzymes, ARG-1 and ARG-2; they are functionally similar, but their coding genes, tissue distribution, subcellular localization, and molecular regulation are distinct.
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