ArticleAmerican journal of physiology. Renal physiology2021
Synaptopodin deficiency exacerbates kidney disease in a mouse model of Alport syndrome.
Article in American journal of physiology. Renal physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 22 citations in OpenAlex.
- Sirt6 ameliorates high glucose-induced podocyte cytoskeleton remodeling via the PI3K/AKT signaling pathway.Renal failure · 2024Article
- The podocytes' inflammatory responses in experimental GN are independent of canonical MYD88-dependent toll-like receptor signaling.Scientific reports · 2024Article
- Klotho Stabilizes the Podocyte Actin Cytoskeleton in Idiopathic Membranous Nephropathy through Regulating the TRPC6/CatL Pathway.American journal of nephrology · 2024Article
- iPSC-derived type IV collagen α5-expressing kidney organoids model Alport syndrome.Communications biology · 2023Article
- Review
- Store-operated CaExperimental biology and medicine (Maywood, N.J.) · 2023Review
- Ion channels and channelopathies in glomeruli.Physiological reviews · 2023Review
- Molecular landscapes of glioblastoma cell lines revealed a group of patients that do not benefit fromFrontiers in neuroscience · 2023Article
- An ex vivo culture model of kidney podocyte injury reveals mechanosensitive, synaptopodin-templating, sarcomere-like structures.Science advances · 2022Article
- Synaptopodin stress fiber and contractomere at the epithelial junction.The Journal of cell biology · 2022Article
- Novel Keap1-Nrf2 Protein-Protein Interaction Inhibitor UBE-1099 Ameliorates Progressive Phenotype in Alport Syndrome Mouse Model.Kidney360 · 2022Article
- TAZ is important for maintenance of the integrity of podocytes.American journal of physiology. Renal physiology · 2022Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Synaptopodin (Synpo) is an actin-associated protein in podocyte foot processes. By generating mice that completely lack Synpo, we previously showed that Synpo is dispensable for normal kidney function. However, lack of Synpo worsened adriamycin-induced nephropathy, indicating a protective role for Synpo in injured podocytes. Here, we investigated whether lack of Synpo directly impacts a genetic disease, Alport syndrome (AS), because Synpo is reduced in podocytes of affected humans and mice; whether this is merely an association or pathogenic is unknown. We used collagen type IV-α
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Registered trials
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