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- W4236029603 abstract "The aging of pancreatic β-cells may undermine their ability to compensate for insulin resistance, leading to the development of type 2 diabetes (T2D). Aging β-cells acquire markers of cellular senescence and develop a senescence-associated secretory phenotype (SASP) that can lead to senescence and dysfunction of neighboring cells through paracrine actions, contributing to b-cell failure. Herein, we defined the β-cell SASP signature based on unbiased proteomic analysis of conditioned media of cells obtained from mouse and human senescent β-cells and a chemically-induced mouse model of DNA damage capable of inducing SASP. These experiments revealed that the β-cell SASP is enriched for factors associated with inflammation, cellular stress response, and extracellular matrix remodeling across species. Multiple SASP factors were transcriptionally upregulated in models of β-cell senescence, aging, insulin resistance and T2D. Single-cell transcriptomic analysis of islets from an <i>in vivo</i> mouse model of reversible insulin resistance indicated unique and partly reversible changes in β-cell subpopulations associated with senescence. Collectively, these results demonstrate the unique secretory profile of senescent b-cells and its potential implication in health and disease." @default.
- W4236029603 created "2022-05-12" @default.
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- W4236029603 date "2021-03-05" @default.
- W4236029603 modified "2023-09-25" @default.
- W4236029603 title "Unique Human and Mouse β-cell Senescence-Associated Secretory Phenotype (SASP) Reveal Conserved Signaling Pathways and Heterogeneous Factors" @default.
- W4236029603 doi "https://doi.org/10.2337/figshare.14125511" @default.
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