ArticleKidney international2016
Loss of Glis2/NPHP7 causes kidney epithelial cell senescence and suppresses cyst growth in the Kif3a mouse model of cystic kidney disease.
Article in Kidney international, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 42 citations in OpenAlex.
- Fisetin as a nutritional senotherapeutic: mechanisms, translational promise, and lessons from chronic kidney disease.Frontiers in nutrition · 2026Review
- The DNA-PKcs-primary cilia axis maintains ionizing radiation-induced senescence in tumor cells.Acta biochimica et biophysica Sinica · 2025Article
- Metabolic reprogramming in polycystic kidney disease and other renal ciliopathies.EMBO molecular medicine · 2025Review
- Use of patient-derived cell models for characterization of compound heterozygous hypomorphic C2CD3 variants in a patient with isolated nephronophthisis.Human molecular genetics · 2025Article
- From premature birth to premature kidney disease: does accelerated aging play a role?Pediatric nephrology (Berlin, Germany) · 2024Review
- Glis2 is an early effector of polycystin signaling and a target for therapy in polycystic kidney disease.Nature communications · 2024Article
- High caspase 3 and vulnerability to dual BCL2 family inhibition define ETO2::GLIS2 pediatric leukemia.Leukemia · 2023Article
- Review
- Identification of a Crosstalk among TGR5, GLIS2, and TP53 Signaling Pathways in the Control of Undifferentiated Germ Cell Homeostasis and Chemoresistance.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Cilia-Localized Counterregulatory Signals as Drivers of Renal Cystogenesis.Frontiers in molecular biosciences · 2022Review
- An updated SYSCILIA gold standard (SCGSv2) of known ciliary genes, revealing the vast progress that has been made in the cilia research field.Molecular biology of the cell · 2021Review
- Nephronophthisis-Pathobiology and Molecular Pathogenesis of a Rare Kidney Genetic Disease.Genes · 2021Review
- Renal Ciliopathies: Sorting Out Therapeutic Approaches for Nephronophthisis.Frontiers in cell and developmental biology · 2021Review
- Transcription factor GLIS3: Critical roles in thyroid hormone biosynthesis, hypothyroidism, pancreatic beta cells and diabetes.Pharmacology & therapeutics · 2020Review
- Review
- Silica Perturbs Primary Cilia and Causes Myofibroblast Differentiation during Silicosis by Reduction of the KIF3A-Repressor GLI3 Complex.Theranostics · 2020Article
- Innate Immune Signaling Contributes to Tubular Cell Senescence in the Glis2 Knockout Mouse Model of Nephronophthisis.The American journal of pathology · 2020Article
- Characterisation of transcription factor profiles in polycystic kidney disease (PKD): identification and validation of STAT3 and RUNX1 in the injury/repair response and PKD progression.Journal of molecular medicine (Berlin, Germany) · 2019Article
- Unexpected Activities in Regulating Ciliation Contribute to Off-target Effects of Targeted Drugs.Clinical cancer research : an official journal of the American Association for Cancer Research · 2019Article
- Towards minimally-invasive, quantitative assessment of chronic kidney disease using optical spectroscopy.Scientific reports · 2019Article
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
Enlargement of kidney tubules is a common feature of multiple cystic kidney diseases in humans and mice. However, while some of these pathologies are characterized by cyst expansion and organ enlargement, in others, progressive interstitial fibrosis and kidney atrophy prevail. The Kif3a knockout mouse is an established non-orthologous mouse model of cystic kidney disease. Conditional inactivation of Kif3a in kidney tubular cells results in loss of primary cilia and rapid cyst growth. Conversely, loss of function of the gene GLIS2/NPHP7 causes progressive kidney atrophy, interstitial inflammatory infiltration, and fibrosis. Kif3a null tubular cells have unrestrained proliferation and reduced stabilization of p53 resulting in a loss of cell cycle arrest in the presence of DNA damage. In contrast, loss of Glis2 is associated with activation of checkpoint kinase 1, stabilization of p53, and induction of cell senescence. Interestingly, the cystic phenotype of Kif3a knockout mice is partially rescued by genetic ablation of Glis2 and pharmacological stabilization of p53. Thus, Kif3a is required for cell cycle regulation and the DNA damage response, whereas cell senescence is significantly enhanced in Glis2 null cells. Hence, cell senescence is a central feature in nephronophthisis type 7 and Kif3a is unexpectedly required for efficient DNA damage response and cell cycle arrest.
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