Rapamycin decreases DNA damage accumulation and enhances cell growth of WRN-deficient human fibroblasts.

[werner syndrome]

Werner syndrome (WS ), caused by mutations at the WRN helicase gene , is a progeroid syndrome characterized by multiple features consistent with accelerated aging . Aberrant double -strand DNA damage repair leads to genomic instability and reduced replicative lifespan of somatic cells . We observed increased autophagy in WRN knockdown cells ; this was further increased by short -term rapamycin treatment . Long -term rapamycin treatment resulted in improved growth rate , reduced accumulation of DNA damage foci and improved nuclear morphology ; autophagy markers were reduced to near-normal levels , possibly due to clearance of damaged proteins . These data suggest that protein aggregation plays a role in the development of WS phenotypes and that the mammalian target of rapamycin complex 1 pathway is a potential therapeutic target of WS .

Diseases
Validation

Diseases presenting "potential therapeutic target" symptom

alexander disease

canavan disease

dedifferentiated liposarcoma

esophageal squamous cell carcinoma

familial hypocalciuric hypercalcemia

familial mediterranean fever

heparin-induced thrombocytopenia

krabbe disease

liposarcoma

lymphangioleiomyomatosis

primary effusion lymphoma

well-differentiated liposarcoma

werner syndrome

wiskott-aldrich syndrome

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