ArticleRedox biology2019
Fragmentation of kidney epithelial cell primary cilia occurs by cisplatin and these cilia fragments are excreted into the urine.
Article in Redox biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- Protective Effect of Mannitol on Cisplatin-Induced Nephrotoxicity: A Systematic Review and Meta-Analysis.Frontiers in oncology · 2021Pooled it
- Diarylpropionitrile, a selective agonist of estrogen receptor β, protects the kidney against ischemia-reperfusion injury and enhances the repair of tubular epithelial cells.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Extracellular stressors change BBSome expression of benign mesothelial and primary pleural mesothelioma cells and affect cell adhesion and migration.Physiological reports · 2026Article
- Persistent subclinical renal injury in female rats following renal ischemia-reperfusion injury.Clinical science (London, England : 1979) · 2025Article
- High water intake induces primary cilium elongation in renal tubular cells.Kidney research and clinical practice · 2024Article
- Cisplatin-induced oxPAPC release enhances MDSCs infiltration into LL2 tumour tissues through MCP-1/CCL2 and LTB4/LTB4R pathways.Cell proliferation · 2024Article
- Shortening of primary cilia length is associated with urine concentration in the kidneys.Kidney research and clinical practice · 2023Article
- Rac1 inhibition protects the kidney against kidney ischemia/reperfusion through the inhibition of macrophage migration.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2023Article
- Article
- Annexin A2 plays a key role in protecting against cisplatin-induced AKI through β-catenin/TFEB pathway.Cell death discovery · 2022Article
- Trilobatin, an Active Dihydrochalcone fromACS omega · 2022Article
- Tubular Mitochondrial Dysfunction, Oxidative Stress, and Progression of Chronic Kidney Disease.Antioxidants (Basel, Switzerland) · 2022Review
- Short-term control of diet affects cisplatin-induced acute kidney injury through modulation of mitochondrial dynamics and mitochondrial GSH.Physiological reports · 2022Article
- Cilia proteins are biomarkers of altered flow in the vasculature.JCI insight · 2022Article
- Mitochondrial Dysfunction: An Emerging Link in the Pathophysiology of Cardiorenal Syndrome.Frontiers in cardiovascular medicine · 2022Review
- Penicilliumin B Protects against Cisplatin-Induced Renal Tubular Cell Apoptosis through Activation of AMPK-Induced Autophagy and Mitochondrial Biogenesis.Kidney diseases (Basel, Switzerland) · 2021Article
- Review
- Immunochromatographic assay to detect α-tubulin in urine for the diagnosis of kidney injury.Journal of clinical laboratory analysis · 2020Article
- An Inhibitor of DRP1 (Mdivi-1) Alleviates LPS-Induced Septic AKI by Inhibiting NLRP3 Inflammasome Activation.BioMed research international · 2020Article
- Primary cilia mediate mitochondrial stress responses to promote dopamine neuron survival in a Parkinson's disease model.Cell death & disease · 2019Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The primary cilium, which protrudes from the cell surface, is associated with the pathogenesis of various diseases, including acute kidney injury (AKI). Primary cilium length dynamically changes during the progression of diseases. However, its relevance in disease and the underlying mechanism are largely unknown. In this study, we investigated the role of primary cilia in AKI induced by cisplatin, an effective anticancer drug, and the underlying mechanisms. In addition, we evaluated the usefulness of length alteration and deciliation of primary cilia into the urine for the diagnosis of AKI. Cisplatin induced shortening, elongation, and normalization of the primary cilia in kidney epithelial cells over time. During shortening, primary cilia fragments and ciliary proteins were excreted into the urine. During deciliation, cell proliferation and the expression of cyclin-dependent kinase inhibitor and proliferating cell nuclear antigen were not significantly changed. Shortening and deciliation of primary cilia were observed before significant increases in plasma creatinine and blood urea nitrogen concentration occurred. Pretreatment with Mito-Tempo, a mitochondria-targeted antioxidant, prevented cisplatin-induced primary cilium shortening and inhibited the increases in superoxide formation, lipid peroxidation, blood urea nitrogen, and tissue damage. In contrast, isocitrate dehydrogenase 2 (Idh2) gene deletion, which results in defect of the NADPH-associated mitochondrial antioxidant system, exacerbated cisplatin-induced changes in mice. Taken together, our findings demonstrate that cisplatin induces deciliation into the urine and antioxidant treatment prevents this deciliation, renal dysfunction, and tissue damage after cisplatin injection. These results suggest that cisplatin-induced AKI is associated with primary cilia and urine primary cilia proteins might be a non-invasive biomarker of kidney injury.
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