ArticleThe American journal of pathology2020
Innate Immune Signaling Contributes to Tubular Cell Senescence in the Glis2 Knockout Mouse Model of Nephronophthisis.
Article in The American journal of pathology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 29 citations in OpenAlex.
- Inhibition of MyD88 in Tubular Epithelial Cells Alleviates the Cellular Senescence in Sepsis-Associated Acute Kidney Injury.Inflammation · 2026Article
- Targeting GLP-1 Signaling Ameliorates Cystogenesis in a Zebrafish Model of Nephronophthisis.International journal of molecular sciences · 2025Article
- Update of cellular senescence in kidney fibrosis: from mechanism to potential interventions.Frontiers of medicine · 2025Review
- Renal aging and its consequences: navigating the challenges of an aging population.Frontiers in pharmacology · 2025Review
- A comparative transcriptomics analysis of mammalian and non-mammalian acute kidney injury (AKI) models.Frontiers in cell and developmental biology · 2025Article
- From premature birth to premature kidney disease: does accelerated aging play a role?Pediatric nephrology (Berlin, Germany) · 2024Review
- Aquaporin 1 is renoprotective in septic acute kidney injury by attenuating inflammation, apoptosis and fibrosis through inhibition of P53 expression.Frontiers in immunology · 2024Article
- Identification of renal cyst cells of type I Nephronophthisis by single-nucleus RNA sequencing.Frontiers in cell and developmental biology · 2023Article
- Cellular senescence and acute kidney injury.Pediatric nephrology (Berlin, Germany) · 2022Review
- Remote ischemic postconditioning protects against crush-induced acute kidney injury via down-regulation of apoptosis and senescence.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2022Article
- Review
- p75Neurotoxicity research · 2022Article
- Neutrophils induce paracrine telomere dysfunction and senescence in ROS-dependent manner.The EMBO journal · 2021Article
- Renal Ciliopathies: Sorting Out Therapeutic Approaches for Nephronophthisis.Frontiers in cell and developmental biology · 2021Review
- Acute kidney injury and maladaptive tubular repair leading to renal fibrosis.Current opinion in nephrology and hypertension · 2020Review
- Review
Corrections and comments
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Authors and funding
16 authors at 7 institutions in 2 countries.
Funding
Abstract
Nephronophthisis (NPHP), the leading genetic cause of end-stage renal failure in children and young adults, is a group of autosomal recessive diseases characterized by kidney-cyst degeneration and fibrosis for which no therapy is currently available. To date, mutations in >25 genes have been identified as causes of this disease that, in several cases, result in chronic DNA damage in kidney tubular cells. Among such mutations, those in the transcription factor-encoding GLIS2 cause NPHP type 7. Loss of function of mouse Glis2 causes senescence of kidney tubular cells. Senescent cells secrete proinflammatory molecules that induce progressive organ damage through several pathways, among which NF-κB signaling is prevalent. Herein, we show that the NF-κB signaling is active in Glis2 knockout kidney epithelial cells and that genetic inactivation of the toll-like receptor (TLR)/IL-1 receptor or pharmacologic elimination of senescent cells (senolytic therapy) reduces tubule damage, fibrosis, and apoptosis in the Glis2 mouse model of NPHP. Notably, in Glis2, Tlr2 double knockouts, senescence was also reduced and proliferation was increased, suggesting that loss of TLR2 activity improves the regenerative potential of tubular cells in Glis2 knockout kidneys. Our results further suggest that a combination of TLR/IL-1 receptor inhibition and senolytic therapy may delay the progression of kidney disease in NPHP type 7 and other forms of this disease.
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