Repeated low-dose cisplatin exposure induces kidney fibroblast-to-myofibroblast transition via G2/M arrest and cellular senescence, driving chronic fibrosis.
Repeated low-dose cisplatin exposure induces kidney fibroblast-to-myofibroblast transition, providing a clinically relevant in vitro model for studying cisplatin-induced chronic kidney disease.
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Cisplatin is a widely used chemotherapeutic agent for solid tumors, but its cumulative nephrotoxicity often progresses to chronic kidney disease (CKD). Although the mechanisms underlying cisplatin-induced acute kidney injury have been extensively studied, the cellular responses leading to chronic fibrosis remain poorly understood. In this study, we established a clinically relevant in vitro model of CKD by repeatedly exposing rat kidney fibroblasts (NRK-49F) to low-dose cisplatin (RLDC).
YU et al. (Wed,) reported a other. Repeated low-dose cisplatin exposure induces kidney fibroblast-to-myofibroblast transition via G2/M arrest and cellular senescence, driving chronic fibrosis.