ArticleAdvanced healthcare materials2026
A Human Kidney Tubuloid Model of Repeated Cisplatin-Induced Cellular Senescence and Fibrosis for Drug Screening.
Article in Advanced healthcare materials, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- Effect of the µ-Diphosphine Bridging Ligand on the Cytotoxic Activity of Homodinuclear Ruthenium Complexes.Molecules (Basel, Switzerland) · 2026Article
- A Human Kidney Tubuloid Model of Repeated Cisplatin-Induced Cellular Senescence and Fibrosis for Drug Screening.Advanced healthcare materials · 2026Article
- Translational Potential: Kidney Tubuloids in Precision Medicine and Regenerative Nephrology.Pharmaceutics · 2026Article
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Authors and funding
21 authors.
Funding
Abstract
In advancing pathophysiological models to assess renal drug responses, kidney organoids derived from human pluripotent stem cells mark notable progress. However, replicating aging- and senescence-related pathologies remains a challenge. In this study, an alternative model is introduced using "tubuloids"-epithelial-like structures generated from primary human renal proximal tubular epithelial cells (hRPTECs) isolated from resected human kidneys. Bulk RNA-seq deconvolution confirmed that tubuloids are highly differentiated and predominantly composed of proximal tubule-like cells. Exposure to cisplatin increased γH2AX, Kidney Injury Molecule-1, and Cleaved Caspase-3, markers for DNA damage response, epithelial damage, and apoptosis, respectively. Repeated cisplatin administration resulted in the upregulation of senescence markers and secretion of inflammatory cytokines, consistent with a senescence-associated secretory phenotype (SASP). Supernatants from cisplatin-treated tubuloids triggered myofibroblast activation, suggesting early fibrotic changes. A hRPTEC-derived tubuloid model of cisplatin-induced kidney injury is successfully developed that mimics senescence, SASP, and fibrosis-hallmarks of chronic kidney disease. This model offers a promising human-relevant platform for studying renal epithelial responses and drug screening.
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Registered trials
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