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Cellular senescence is characterized by a stable cell cycle arrest and a hypersecretory, proinflammatory phenotype in response to various stress stimuli. Traditionally, this state has been viewed as a tumor-suppressing mechanism that prevents the proliferation of damaged cells while activating the immune response for their clearance. However, senescence is increasingly recognized as a contributing factor to tumor progression.
View Article and Find Full Text PDFChloride intracellular channel CLIC3 mediates fibroblast cellular senescence by interacting with ERK7.
Commun Biol
January 2025
Laboratory of Intensive Care, Laboratory for Prevention and Translation of Geriatric Diseases, The Affiliated Hospital of Yangzhou University, Yangzhou, China.
Cellular senescence (CS) is recognized as a critical driver of aging and age-related disorders. Recent studies have emphasized the roles of ion channels as key mediators of CS. Nonetheless, the roles and regulatory mechanisms of chloride intracellular channels (CLICs) during CS remain largely unexplored.
View Article and Find Full Text PDFCDK8 mediated inflammatory microenvironment aggravates osteoarthritis progression.
J Adv Res
January 2025
Introduction: Cyclin-Dependent Kinase 8 (CDK8), a CDK family member, regulates the development of inflammatory processes through transcriptional activation. The involvement of CDK8 in osteoarthritis (OA) progression is not yet understood.
Objectives: This study aims to investigate whether CDK8, through its transcriptional regulatory functions, collaborates with NF-κB in chondrocytes to regulate the transcription of senescence-associated secretory phenotype (SASP) genes, thereby exacerbating the inflammatory microenvironment in the progression of osteoarthritis (OA), and to explore the specific mechanisms involved.
Insights into age-related osteoporosis from senescence-based preclinical models and human accelerated aging paradigms.
Mech Ageing Dev
January 2025
Department of Medicine, Divisions of Geriatric Medicine and Gerontology, the Department of Physiology and Biomedical Engineering, and the Robert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, Minnesota. Electronic address:
Preclinical models of age-related osteoporosis have been developed based on the accumulation and clearance of senescent cells. The former include animal models based on telomere dysfunction and focal radiation; the latter based on genetic and pharmacological targeting (i.e.
View Article and Find Full Text PDFBenign prostatic hyperplasia (BPH) is among the most common age-associated diseases in men; however, the contribution of age-related changes in immune cells to BPH is not clear. The current study determined that an age-associated CD8 T cell subset (Taa) with high Granzyme K ( ) and low Granzyme B ( ) gene expression infiltrate aged human prostates and positively correlate with International Prostate Symptom Score (IPSS). A velocity analysis indicated that CD8 T cell differentiation is altered in large BPH prostates compared to small age-matched prostates, favoring Taa accumulation.
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