ArticleKidney international2019
The motor protein Myo1c regulates transforming growth factor-β-signaling and fibrosis in podocytes.
Article in Kidney international, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
19 citing papers in PubMed, 30 citations in OpenAlex.
- SnRNA-seq and genome-wide CRISPR screening define the complete transcriptional trajectory and functional drivers of podocyte stress.Cellular and molecular life sciences : CMLS · 2026Article
- Application of the nephrotoxic serum nephritis model in glomerulonephritis research.Molecular medicine (Cambridge, Mass.) · 2026Review
- MYO1C is a urinary extracellular vesicle biomarker and mediator of podocyte injury in diabetic nephropathy.JCI insight · 2026Article
- A methylome-wide association study of major depression with out-of-sample case-control classification and trans-ancestry comparison.Nature. Mental health · 2025Article
- Liraglutide Promotes Diabetic Wound Healing via Myo1c/Dock5.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Recessive variants in MYO1C as a potential novel cause of proteinuric kidney disease.Pediatric nephrology (Berlin, Germany) · 2024Article
- Myosin1G promotes Nodal signaling to control zebrafish left-right asymmetry.Nature communications · 2024Article
- Recessive variants in MYO1C as a potential novel cause of proteinuric kidney disease.Research square · 2024Article
- Article
- RAB31 in glioma-derived endothelial cells promotes glioma cell invasion via extracellular vesicle-mediated enrichment of MYO1C.FEBS open bio · 2024Article
- Article
- Review
- Urinary Growth Differentiation Factor-15 (GDF15) levels as a biomarker of adverse outcomes and biopsy findings in chronic kidney disease.Journal of nephrology · 2021Article
- Deconvolution of Focal Segmental Glomerulosclerosis Pathophysiology Using Transcriptomics Techniques.Glomerular diseases · 2021Review
- Targeting myosin 1c inhibits murine hepatic fibrogenesis.American journal of physiology. Gastrointestinal and liver physiology · 2021Article
- Loss of Motor Protein MYO1C Causes Rhodopsin Mislocalization and Results in Impaired Visual Function.Cells · 2021Article
- Prognostic Value of Growth Differentiation Factor 15 in Kidney Donors and Recipients.Journal of clinical medicine · 2020Article
- Roles of Myosin-Mediated Membrane Trafficking in TGF-β Signaling.International journal of molecular sciences · 2019Review
- Disruption of the exocyst induces podocyte loss and dysfunction.The Journal of biological chemistry · 2019Article
Corrections and comments
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Authors and funding
17 authors at 6 institutions in 3 countries.
Funding
Abstract
Transforming growth factor-β (TGF-β) is known to play a critical role in the pathogenesis of many progressive podocyte diseases. However, the molecular mechanisms regulating TGF-β signaling in podocytes remain unclear. Using a podocyte-specific myosin (Myo)1c knockout, we demonstrate whether Myo1c is critical for TGF-β-signaling in podocyte disease pathogenesis. Specifically, podocyte-specific Myo1c knockout mice were resistant to fibrotic injury induced by Adriamycin or nephrotoxic serum. Further, loss of Myo1c also protected from injury in the TGF-β-dependent unilateral ureteral obstruction mouse model of renal interstitial fibrosis. Mechanistic analyses showed that loss of Myo1c significantly blunted TGF-β signaling through downregulation of canonical and non-canonical TGF-β pathways. Interestingly, nuclear rather than the cytoplasmic Myo1c was found to play a central role in controlling TGF-β signaling through transcriptional regulation. Differential expression analysis of nuclear Myo1c-associated gene promoters showed that nuclear Myo1c targeted the TGF-β responsive gene growth differentiation factor (GDF)-15 and directly bound to the GDF-15 promoter. Importantly, GDF15 was found to be involved in podocyte pathogenesis, where GDF15 was upregulated in glomeruli of patients with focal segmental glomerulosclerosis. Thus, Myo1c-mediated regulation of TGF-β-responsive genes is central to the pathogenesis of podocyte injury. Hence, inhibiting this process may have clinical application in treating podocytopathies.
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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.