ArticleJCI insight2018
Inducible podocyte-specific deletion of CTCF drives progressive kidney disease and bone abnormalities.
Article in JCI insight, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- The effects of elevated phosphate on the kidney - damaging the gatekeeper.Pflugers Archiv : European journal of physiology · 2026Review
- Role of lactate dehydrogenase A in the regulation of podocyte metabolism and glucose uptake under hyperglycemic conditions.Scientific reports · 2025Article
- A guide to studying 3D genome structure and dynamics in the kidney.Nature reviews. Nephrology · 2025Review
- Renin-angiotensin blockade ameliorates the progression of glomerular injury in podocyte-specific Ctcf knockout mice.Nephrology (Carlton, Vic.) · 2024Article
- Role of biophysics and mechanobiology in podocyte physiology.Nature reviews. Nephrology · 2024Review
- Radiation nephropathy: Mechanisms of injury and recovery in a murine model.Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology · 2023Article
- Renal proximal tubule cells: power and finesse.The Journal of clinical investigation · 2023Article
- A parathyroid hormone/salt-inducible kinase signaling axis controls renal vitamin D activation and organismal calcium homeostasis.The Journal of clinical investigation · 2023Article
- Mouse Models of Mineral Bone Disorders Associated with Chronic Kidney Disease.International journal of molecular sciences · 2023Review
- Single-Cell Transcriptomics Reveal Disrupted Kidney Filter Cell-Cell Interactions after Early and Selective Podocyte Injury.The American journal of pathology · 2022Article
- A clear pathway to tubulointerstitial disease: is an exclusive focus on fibrosis justified?The Journal of clinical investigation · 2021Article
- Selective pharmacological inhibition of the sodium-dependent phosphate cotransporter NPT2a promotes phosphate excretion.The Journal of clinical investigation · 2020Article
- Fibroblast growth factor 23: are we ready to use it in clinical practice?Journal of nephrology · 2020Review
- Transcriptomics: a Solution for Renal Osteodystrophy?Current osteoporosis reports · 2020Review
- FGF23 Actions on Target Tissues-With and Without Klotho.Frontiers in endocrinology · 2018Review
Corrections and comments
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Authors and funding
15 authors at 7 institutions in 3 countries.
Funding
Abstract
Progressive chronic kidney diseases (CKDs) are on the rise worldwide. However, the sequence of events resulting in CKD progression remain poorly understood. Animal models of CKD exploring these issues are confounded by systemic toxicities or surgical interventions to acutely induce kidney injury. Here we report the generation of a CKD mouse model through the inducible podocyte-specific ablation of an essential endogenous molecule, the chromatin structure regulator CCCTC-binding factor (CTCF), which leads to rapid podocyte loss (iCTCFpod-/-). As a consequence, iCTCFpod-/- mice develop severe progressive albuminuria, hyperlipidemia, hypoalbuminemia, and impairment of renal function, and die within 8-10 weeks. CKD progression in iCTCFpod-/- mice leads to high serum phosphate and elevations in fibroblast growth factor 23 (FGF23) and parathyroid hormone that rapidly cause bone mineralization defects, increased bone resorption, and bone loss. Dissection of the timeline leading to glomerular pathology in this CKD model led to the surprising observation that podocyte ablation and the resulting glomerular filter destruction is sufficient to drive progressive CKD and osteodystrophy in the absence of interstitial fibrosis. This work introduces an animal model with significant advantages for the study of CKD progression, and it highlights the need for podocyte-protective strategies for future kidney therapeutics.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.