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We are analyzing https://www.biorxiv.org/content/10.1101/2025.05.07.648438v1.

Title:
A human and mouse subpopulation of senescent β-cells induces pathologic dysfunction through targetable paracrine signaling | bioRxiv
Description:
Cellular senescence is a stress response mechanism marked by irreversible growth arrest, upregulation of antiapoptotic pathways, loss of cellular function, and remodelling of the cellular secretory profile. In both humans and mice, pancreatic β-cells undergo senescence with age and insulin resistance. Targeted removal of senescent cells in mouse models of diabetes improves glucose homeostasis, demonstrating the role β-cell senescence in diabetes progression. In contrast, β-cell senescence also promotes immune surveillance, promoting β-cell survival and function. Thus, a better understanding of senescent cells’ phenotypic and functional heterogeneity is needed to develop effective therapeutic strategies. Herein, we show that subpopulations of senescent β-cells in mice and humans, which were identified through the expression of Cdkn1a (encoding p21Cip1 ) and Cdkn2a (encoding p16Ink4a ) by single-cell RNA sequencing (scRNA-seq), flow cytometry, spatial transcriptomics, and spatial proteomics, exhibit distinct transcriptional and functional identities. The predominant senescent β-cell subpopulation expressed Cdkn1a and was characterized by a lack of glucose responsiveness, high basal insulin secretion, and transcription of canonical SASP factors. The SASP of Cdkn1a -expressing β-cells had non-cell autonomous effects on neighbouring cells. A subset of four SASP factors from Cdkn1a+ cells was sufficient to induce secondary senescence and β-cell dysfunction in vitro . JAK inhibitors (JAK1/2 and JAK1/3) counteracted secondary senescence induction and restored β-cell function in high-fat diet-fed mice and human islets from donors with or without type 2 diabetes. ![Figure][1]</img> ### Competing Interest Statement Part of the work in this manuscript has been submitted for a patent JDP-216 on January 16, 2024, as a US Provisional, 63,621,239. Startup Foundation, https://ror.org/05s31v772 National Institutes of Health, 1R01DK132535, P30DK036836 the Beatson Foundation, 2020-010 The Richard and Susan Smith Family Foundation Award NIH NIDDK, 1R25DK113652 Joslin-BIDMC Post-Bac Program NIH, R37 AG13925, 2UC4DK098085 Hevolution, HF-GRO-23-1199148-3 the Connor Fund Robert and Theresa Ryan the Noaber Foundation Manpei Suzuki Diabetes Foundation, https://ror.org/03pkewe16 Mary K. Iacocca Fellowship NIH/NIA, U54AG075941 [1]: pending:yes
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Topics {✒️}

epidemiology subject categories high-fat diet-fed mice role β-cell senescence clinical trials promoting β-cell survival single-cell rna sequencing iacocca fellowship nih/nia restored β-cell function β-cell senescence β-cell dysfunction org/05s31v772 national institutes cdkn1a-expressing β-cells biorxiv subject category genetics microbiology cell autonomous effects cellular secretory profile epidemiology papers author/funder senescent β-cells reviews induce secondary senescence download figureopen senescent cells’ phenotypic keyword advanced search health-related information juliana alcoforado diniz irreversible growth arrest promotes immune surveillance exhibit distinct transcriptional connor fund robert generous financial support chan zuckerberg initiative imperial college london vrije universiteit amsterdam articles animal behavior org/03pkewe16 mary context senescent cells canonical sasp factors beatson foundation cdkn1a+ cells cellular function mouse subpopulation diabetes progression type 2 diabetes neighbouring cells insulin resistance glucose responsiveness sasp factors

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