ArticleThe Journal of clinical investigation2023
Profilin1 is required for prevention of mitotic catastrophe in murine and human glomerular diseases.
Article in The Journal of clinical investigation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 24 citations in OpenAlex.
- Single-cell and high-resolution spatial profiling of podocytopathies reveals core mechanisms of podocyte injury.Science advances · 2026Article
- Molecular mechanisms and novel therapeutic targets of diabetic kidney disease.Chinese medical journal · 2026Review
- Proteomic analysis of plasma extracellular vesicles for predicting acute kidney injury following laparoscopic radical nephrectomy.Scientific reports · 2026Article
- TRPC6 Inhibition Attenuates Renal Tubulointerstitial Fibrosis via the Reactive Oxygen Species/TXNIP/NLRP3 Signaling Pathway.Kidney & blood pressure research · 2026Article
- Podocytopathies.Nature reviews. Disease primers · 2025Review
- Machine learning-based prediction of tubulointerstitial lesions in diabetic kidney disease: a multicenter validation study.Renal failure · 2025Article
- Diagnostic value of the correlation between urinary MDM2 and podocyte mitotic catastrophe in diabetic kidney disease.Diabetology & metabolic syndrome · 2025Article
- Cell cycle disorders in podocytes: an emerging and increasingly recognized phenomenon.Cell death discovery · 2025Review
- Piezo1, F-Actin Remodeling, and Podocyte Survival and Regeneration.Journal of the American Society of Nephrology : JASN · 2025Article
- CRB2 depletion induces YAP signaling and disrupts mechanosensing in podocytes.American journal of physiology. Renal physiology · 2025Article
- Advanced RPL19-TRAPNatural products and bioprospecting · 2025Article
- Integrins in the kidney - beyond the matrix.Nature reviews. Nephrology · 2025Review
- Modulation of the thiol redox proteome by sugarcane ash-derived silica nanoparticles: insights into chronic kidney disease of unknown etiology.Particle and fibre toxicology · 2025Article
- Podocytes in health and glomerular disease.Frontiers in cell and developmental biology · 2025Review
- The Role of Podocytes in Lupus Pathology.Current rheumatology reports · 2024Review
- Hyperactivation of p53 contributes to mitotic catastrophe in podocytes through regulation of the Wee1/CDK1/cyclin B1 axis.Renal failure · 2024Article
- Regulation of formin INF2 and its alteration in INF2-linked inherited disorders.Cellular and molecular life sciences : CMLS · 2024Review
- INF2 formin variants linked to human inherited kidney disease reprogram the transcriptome, causing mitotic chaos and cell death.Cellular and molecular life sciences : CMLS · 2024Article
- Podocytes from hypertensive and obese mice acquire an inflammatory, senescent, and aged phenotype.American journal of physiology. Renal physiology · 2024Article
- The loss of profilin1 is catastrophic to podocytes.The Journal of clinical investigation · 2023Article
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Authors and funding
21 authors at 3 institutions in 2 countries.
Funding
Abstract
The progression of proteinuric kidney diseases is associated with podocyte loss, but the mechanisms underlying this process remain unclear. Podocytes reenter the cell cycle to repair double-stranded DNA breaks. However, unsuccessful repair can result in podocytes crossing the G1/S checkpoint and undergoing abortive cytokinesis. In this study, we identified Pfn1 as indispensable in maintaining glomerular integrity - its tissue-specific loss in mouse podocytes resulted in severe proteinuria and kidney failure. Our results suggest that this phenotype is due to podocyte mitotic catastrophe (MC), characterized histologically and ultrastructurally by abundant multinucleated cells, irregular nuclei, and mitotic spindles. Podocyte cell cycle reentry was identified using FUCCI2aR mice, and we observed altered expression of cell-cycle associated proteins, such as p21, p53, cyclin B1, and cyclin D1. Podocyte-specific translating ribosome affinity purification and RNA-Seq revealed the downregulation of ribosomal RNA-processing 8 (Rrp8). Overexpression of Rrp8 in Pfn1-KO podocytes partially rescued the phenotype in vitro. Clinical and ultrastructural tomographic analysis of patients with diverse proteinuric kidney diseases further validated the presence of MC podocytes and reduction in podocyte PFN1 expression within kidney tissues. These results suggest that profilin1 is essential in regulating the podocyte cell cycle and its disruption leads to MC and subsequent podocyte loss.
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