Key result
Repeated low-dose cisplatin drives chronic kidney fibrosis by inducing fibroblast transition via G2/M arrest and senescence.
Why the study?
Cisplatin nephrotoxicity often progresses to CKD, but the cellular responses leading to chronic fibrosis remain poorly understood.
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.
Answers are grounded in this paper and cite their sources.
Supports caution with repeated low-dose cisplatin in cancer care; extends mechanistic insights and provides a clinically relevant in vitro model for CKD.
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).
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YU et al. (2026) studied this question. Repeated low-dose cisplatin exposure induces kidney fibroblast-to-myofibroblast transition via G2/M arrest and cellular senescence, driving chronic fibrosis.
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