Working model of the mechanism by which counteracting lysosome defects alleviates cellular senescence in HGPS (IMAGE)
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In HGPS cells, progerin can be expelled from the nucleus into the cytoplasm via nuclear envelope budding and degraded through lysosomes. However, lysosome defects, which impair progerin clearance, occur in progeria cells. PMA or Torin 1 treatment promotes the nuclear translocation of TFEB, activates lysosome biogenesis and progerin clearance in HGPS cells, and accordingly alleviates senescence phenotypes, including DNA damage, cell cycle arrest, low proliferation ability and SASP. (PMA, phorbol 12-myristate 13-acetate; SASP, senescence-associated secretory phenotype.)
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