ArticleThe Journal of clinical investigation2022
Decoupling dedifferentiation and G2/M arrest in kidney fibrosis.
Article in The Journal of clinical investigation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 5 citations in OpenAlex.
- From AKI to CKD mechanisms of maladaptive repair and disease progression.International urology and nephrology · 2026Review
- Transcriptomic and Metabolomic Analysis Reveals That Polystyrene Microplastics Exacerbate Cadmium-Induced Liver Damage in Mice Associated with AMPK-FOXO-Mediated Energy Metabolism Dysregulation.Veterinary sciences · 2026Article
- PHLDA1 is a shared diagnostic and key mediator of inflammatory fibrosis in heart and kidney.Frontiers in immunology · 2026Article
- Transcriptomic analysis of Paraoxonase 1 expression in hepatocellular carcinoma and its potential impact on tumor immunity.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025Article
- 5-Hydroxytryptamine 1F Receptor Agonist Lasmiditan Differentially Regulates Successful Repair and Failed Repair Genes in a Mouse Model of Acute Kidney Injury.ACS pharmacology & translational science · 2024Article
- Phosphorylation of PBK at Thr9 by CDK5 correlates with invasion of prolactinomas.CNS neuroscience & therapeutics · 2024Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Understanding the cellular mechanisms underlying chronic kidney disease (CKD) progression is required to develop effective therapeutic approaches. In this issue of the JCI, Taguchi, Elias, et al. explore the relationship between cyclin G1 (CG1), an atypical cyclin that induces G2/M proximal tubule cell cycle arrest, and epithelial dedifferentiation during fibrogenesis. While CG1-knockout mice were protected from fibrosis and had reduced G2/M arrest, protection was unexpectedly independent of induction of G2/M arrest. Rather, CG1 drove fibrosis by regulating maladaptive dedifferentiation in a CDK5-dependent mechanism. These findings highlight the importance of maladaptive epithelial dedifferentiation in kidney fibrogenesis and identify CG1/CDK5 signaling as a therapeutic target in CKD progression.
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Registered trials
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