Abstract
Premature Aging Cells from patients with Hutchinson-Gilford progeria syndrome (HGPS) have defects in nuclear architecture that lead to premature cellular senescence. Larrieu et al. investigated the mechanisms by which a small molecule called remodelin improves the phenotype of HGPS cells (see the Focus by Wilson). Remodelin restored a nuclear import pathway mediated by Transportin-1 that was defective in HGPS cells, thereby delaying premature senescence. These results could also be applied to delay cellular senescence in cells derived from aged healthy individuals. Sci. Signal. 11 , eaar5401; see also eaat9448 (2018).
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