Bleomycin-treated myoblasts undergo p21-associated cellular senescence and have severely impaired differentiation.

ABSTRACT: As we age, the ability to regenerate and repair skeletal muscle damage declines, partially due to increasing dysfunction of muscle resident stem cells-satellite cells (SC). Recent evidence implicates cellular senescence, which is the irreversible arrest of proliferation, as a potentiator of SC impairment during aging. However, little is known about the role of senescence in SC, and there is a large discrepancy in senescence classification within skeletal muscle. The purpose of this study was to develop a model of senescence in skeletal muscle myoblasts and identify how common senescence-associated biomarkers respond. Low-passage C₂C₁₂ myoblasts were treated with bleomycin or vehicle and then evaluated for cytological and molecular senescence markers, proliferation sta

SUBMITTER: Kamal M 

PROVIDER: S-EPMC10828175 | biostudies-literature | 2024 Apr

REPOSITORIES: biostudies-literature