Werner Syndrome: Symptoms, Hallmarks of Aging, Molecular Mechanisms and Therapeutic Pathway Inhibitors
DOI:
https://doi.org/10.18192/osurj.v5i1.8073Abstract
Werner Syndrome (WS) is a rare autosomal recessive progeroid disorder characterized by accelerated aging and the premature onset of age-related conditions, such as stunted growth, cataracts, cardiovascular disease, malignancies, sarcopenia, osteoporosis, and diabetes. Clinical disease manifestations typically begin in adolescence to early adulthood, and result in a reduced lifespan compared to healthy individuals. WS arises from loss-of-function mutations in the WRN gene, which encodes a RecQ family helicase that has implications in DNA repair, replication, and telomere maintenance. Deficiency in functional RecQ helicase activity results in dysfunction that links WS to the hallmarks of aging, including genomic instability, telomere attrition, and premature cellular senescence. To date, there is no cure for WS, with current therapies primarily focusing on disease management through inhibition of important proteins in aging- and stress-related signaling pathways, namely mTOR and p38 MAPK. These emerging approaches have shown promising results in cellular models, but have yet to be tested in human clinical studies. This review therefore examines WS as a potential model for understanding the mechanisms of aging, and the implications of existing findings for informing new therapeutic strategies.
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