ArticleScientific reports2021
Creation of X-linked Alport syndrome rat model with Col4a5 deficiency.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- A nonsense mutation in the Mocos gene induces xanthinuria, obstructive nephropathy, and anemia in rats.Experimental animals · 2026Article
- Gene modification: Exploring the potential in treating kidney diseases.Pharmacological research · 2026Review
- CRISPR and gene editing for kidney diseases: where are we?Clinical kidney journal · 2025Review
- Construction of arginine vasopressin receptor 2-deficient rats by the rGONAD method.Clinical and experimental nephrology · 2025Article
- Experimental models for preclinical research in kidney disease.Zoological research · 2024Review
- Alport Syndrome: A Comprehensive Review.Cureus · 2023Review
- A mouse model for X-linked Alport syndrome induced by Del-ATGG in theFrontiers in medicine · 2023Article
- Article
- Novel heterozygous mutation inFrontiers in genetics · 2022Article
- GONAD: A new method for germline genome editing in mice and rats.Development, growth & differentiation · 2021Article
- Temporal Transcriptomics Leads From Discovery to in Vivo Validation: COL4A3/COL4A6/ COL4A5 and ITGA8 as Novel Arthrofibrosis Biomarkers in Post-traumatic Joint Contracture.Dose-response : a publication of International Hormesis SocietyArticle
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alport syndrome is an inherited chronic human kidney disease, characterized by glomerular basement membrane abnormalities. This disease is caused by mutations in COL4A3, COL4A4, or COL4A5 gene. The knockout mice for Col4α3, Col4α4, and Col4α5 are developed and well characterized for the study of Alport syndrome. However, disease progression and effects of pharmacological therapy depend on the genetic variability. This model was reliable only to mouse. In this study, we created a novel Alport syndrome rat model utilizing the rGONAD technology, which generated rat with a deletion of the Col4α5 gene. Col4α5 deficient rats showed hematuria, proteinuria, high levels of BUN, Cre, and then died at 18 to 28 weeks of age (Hemizygous mutant males). Histological and ultrastructural analyses displayed the abnormalities including parietal cell hyperplasia, mesangial sclerosis, and interstitial fibrosis. Then, we demonstrated that α3/α4/α5 (IV) and α5/α5/α6 (IV) chains of type IV collagen disrupted in Col4α5 deficient rats. Thus, Col4α5 mutant rat is a reliable candidate for the Alport syndrome model for underlying the mechanism of kidney diseases and further identifying potential therapeutic targets for human renal diseases.
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