Nucleolar stress facilitates islet β cell senescence via hijacking the DNA damage response pathways.
Abstract
Senescence is a crucial contributor to pancreatic β cell dysfunction during diabetes progression. Herein, we demonstrated that nucleolar stress, a stress event resulting from disrupted ribosomal RNA (rRNA) synthesis, drives β cell senescence. Senescent β cells exhibited altered nucleolar morphology and redistribution of the nucleolar protein nucleophosmin (NPM)
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Research summary
Nucleolar stress drives β cell senescence through the hijacking of DNA damage response pathways. This research addresses a mechanism contributing to cellular senescence, which is a key factor in aging and age-related diseases, particularly in the context of diabetes.
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