ArticleCells2022
Repeated Administration of Cisplatin Transforms Kidney Fibroblasts through G2/M Arrest and Cellular Senescence.
Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 18 citations in OpenAlex.
- An Acidic Tubulointerstitial Microenvironment Delays Cell-Cycle Progression in Proximal Tubule Cells and Fibroblasts and Synergizes With Lactate to Drive Phenotypic Alterations.Acta physiologica (Oxford, England) · 2026Article
- Pre-treatment with 2-mercaptoethanol attenuates ferroptosis-associated redox imbalance and inflammatory responses, but not tubulointerstitial fibrosis, in unilateral ureteral obstruction.Pharmacological reports : PR · 2026Article
- Phenolic-Enriched Fractions ofCurrent issues in molecular biology · 2026Article
- Functional Characterization ofDiseases (Basel, Switzerland) · 2026Article
- Poor prognosis of acute kidney injury superimposed on chronic kidney disease: potential mechanisms, risk factors and novel biomarkers.Frontiers in molecular biosciences · 2026Review
- Inflammation: The Pathological Axis of Cisplatin-Induced Renal Injury.Journal of inflammation research · 2026Review
- The role of cisplatin in modulating the tumor immune microenvironment and its combination therapy strategies: a new approach to enhance anti-tumor efficacy.Annals of medicine · 2025Review
- Palladium Complex-Supported Silica Nanocarriers: Enhancing Therapeutic Efficacy and Reducing Curcumin Toxicity in Breast Cancer.Journal of cellular and molecular medicine · 2025Article
- DCAF2 regulates the proliferation and differentiation of mouse progenitor spermatogonia by targeting p21 and thymine DNA glycosylase.Cell proliferation · 2024Article
- Article
- Senescence in the bone marrow microenvironment: A driver in development of therapy-related myeloid neoplasms.Journal of bone oncology · 2024Article
- The AKI-to-CKD Transition: The Role of Uremic Toxins.International journal of molecular sciences · 2023Review
- The Potential of Senescence as a Target for Developing Anticancer Therapy.International journal of molecular sciences · 2023Review
- HDAC6 Inhibition Alleviates Ischemia- and Cisplatin-Induced Acute Kidney Injury by Promoting Autophagy.Cells · 2022Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cisplatin is a potent chemotherapeutic used for the treatment of many types of cancer, but it has nephrotoxic side effects leading to acute kidney injury and subsequently chronic kidney disease (CKD). Previous work has focused on acute kidney tubular injury induced by cisplatin, whereas the chronic sequelae post-injury has not been well-explored. In the present study, we established a kidney fibroblast model of CKD induced by repeated administration of cisplatin (RAC) as a clinically relevant model. In NRK-49F rat kidney fibroblasts, RAC upregulated α-smooth muscle actin (α-SMA) and fibronectin proteins, suggesting that RAC induces kidney fibroblast-to-myofibroblast transformation. RAC also enhanced cell size, including the cell attachment surface area, nuclear area, and cell volume. Furthermore, RAC induced p21 expression and senescence-associated β-galactosidase activity, suggesting that kidney fibroblasts exposed to RAC develop a senescent phenotype. Inhibition of p21 reduced cellular senescence, hypertrophy, and myofibroblast transformation induced by RAC. Intriguingly, after RAC, kidney fibroblasts were arrested at the G2/M phase. Repeated treatment with paclitaxel as an inducer of G2/M arrest upregulated p21, α-SMA, and fibronectin in the kidney fibroblasts. Taken together, these data suggest that RAC transforms kidney fibroblasts into myofibroblasts through G2/M arrest and cellular senescence.
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