ReviewPediatric nephrology (Berlin, Germany)2025
Mechanisms of podocyte injury in genetic kidney disease.
Review in Pediatric nephrology (Berlin, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- The landscape of allele-specific expression in human kidneys.Science advances · 2026Article
- Treatment outcomes and ongoing pediatric trials in steroid-resistant nephrotic syndrome.Pediatric nephrology (Berlin, Germany) · 2026Review
- Piezo1 and podocyte mechano-sensing in hypertensive nephropathy.Hypertension research : official journal of the Japanese Society of Hypertension · 2026Article
- Podocyte-specific deletion of mechanochannel Piezo1 exacerbates proteinuria and podocyte injury in mouse hypertensive nephropathy.Hypertension research : official journal of the Japanese Society of Hypertension · 2026Article
- Drugs to Slow Progression of Chronic Kidney Disease: It Is a Whole New World!Kidney & blood pressure research · 2026Review
- Comprehensive snRNA-Seq Datasets of Human and Mouse Podocytopathy Integrated with GWAS of Microalbuminuria.Scientific data · 2025Article
- Podocytes in health and disease: from development to regeneration.Human cell · 2025Review
- The Spectrum of Minimal Change Disease/Focal Segmental Glomerulosclerosis: From Pathogenesis to Proteomic Biomarker Research.International journal of molecular sciences · 2025Review
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Authors and funding
3 authors.
Funding
Abstract
Glomerular diseases are a leading cause of chronic kidney disease worldwide. Both acquired and hereditary glomerulopathies frequently share a common final disease mechanism: disruption of the glomerular filtration barrier, podocyte injury, and ultimately podocyte death and detachment. Over 70 monogenic causes of proteinuric kidney disease have been identified, and most of these genes are highly expressed in podocytes, regulating key processes such as maintenance of the slit diaphragm, regulation of actin cytoskeleton remodeling, and modulation of downstream transcriptional pathways. Collectively, these are increasingly being referred to as hereditary "podocytopathies," in which podocyte injury is the central feature driving proteinuria and kidney dysfunction. In this review, we provide an overview of the monogenic podocytopathies and discuss the molecular mechanisms by which single-gene defects lead to podocyte injury and ultimately glomerulosclerosis. We review how advances in genomic technology and a better understanding of the cell biological basis of disease have led to the development of more targeted and personalized therapeutic strategies, including an overview of small molecule and gene therapy approaches.
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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.