ArticleJournal of the American Society of Nephrology : JASN2008
Podocyte-specific deletion of dicer alters cytoskeletal dynamics and causes glomerular disease.
Article in Journal of the American Society of Nephrology : JASN, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 176 papers, 1 of them a synthesis that pooled it.
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Who cites it
176 citing papers in PubMed, 1 synthesis or guideline pooled it, 321 citations in OpenAlex.
- Role of microRNAs in the Therapeutic Effects of Curcumin in Non-Cancer Diseases.Molecular diagnosis & therapy · 2016Pooled it
- Investigation of urinary miRNA profile changes in amphotericin B-induced nephrotoxicity in C57BL/6 mouse, Sprague-Dawley rats and Beagle dogs.Toxicological sciences : an official journal of the Society of Toxicology · 2025Article
- Research progress on miR-124-3p in the field of kidney disease.BMC nephrology · 2024Review
- Senolytic combination of dasatinib and quercetin protects against diabetic kidney disease by activating autophagy to alleviate podocyte dedifferentiation via the Notch pathway.International journal of molecular medicine · 2024Article
- MicroRNA193a: An Emerging Mediator of Glomerular Diseases.Biomolecules · 2023Review
- Ulinastatin ameliorates podocyte ferroptosis via regulating miR-144-3p/SLC7A11 axis in acute kidney injury.In vitro cellular & developmental biology. Animal · 2023Article
- Urinary Extracellular Vesicles in Chronic Kidney Disease: From Bench to Bedside?Diagnostics (Basel, Switzerland) · 2023Review
- Review
- MicroRNAs in kidney injury and disease.Nature reviews. Nephrology · 2022Review
- Systemic gene therapy with thymosin β4 alleviates glomerular injury in mice.Scientific reports · 2022Article
- The Role ofNon-coding RNA · 2022Article
- MicroRNAs in kidney development and disease.JCI insight · 2022Review
- Stem cell-derived and circulating exosomal microRNAs as new potential tools for diabetic nephropathy management.Stem cell research & therapy · 2022Review
- Podocyte-specific deletion of miR-146a increases podocyte injury and diabetic kidney disease.Frontiers in medicine · 2022Article
- Evaluation of endogenous miRNA reference genes across different zebrafish strains, developmental stages and kidney disease models.Scientific reports · 2021Article
- The role of miR-29 family in disease.Journal of cellular biochemistry · 2021Review
- Functional miR143/145 Cluster Variants and Haplotypes Are Associated with Chronic Kidney Disease: a Preliminary Case-Control Study and Computational Analyses.Applied biochemistry and biotechnology · 2021Article
- Article
- Impact of gestational low-protein intake on embryonic kidney microRNA expression and in nephron progenitor cells of the male fetus.PloS one · 2021Article
- Gestational Low Protein Diet Modulation on miRNA Transcriptome and Its Target During Fetal and Breastfeeding Nephrogenesis.Frontiers in physiology · 2021Article
116 more citing papers are in PubMed but not listed here.
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9 authors at 5 institutions in 3 countries.
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Abstract
MicroRNAs (miRNAs) regulate gene expression by binding the 3' untranslated region of mRNAs. To define their role in glomerular function, miRNA biogenesis was disrupted in mouse podocytes using a conditional Dicer allele. Mutant mice developed proteinuria by 3 wk after birth and progressed rapidly to end-stage kidney disease. Podocyte pathology included effacement, vacuolization, and hypertrophy with crescent formation. Despite normal expression of WT1, podocytes underwent dedifferentiation, exemplified by cytoskeletal disruption with early transcriptional downregulation of synaptopodin. These abnormalities differed from Cd2ap(-/-) mice, indicating they were not a general consequence of glomerular disease. Glomerular labeling of ezrin, moesin, and gelsolin was altered at 3 wk, but expression of nestin and alpha-actinin was unchanged. Abnormal cell proliferation or apoptosis was not responsible for the glomerular injury. Mutant podocytes were incapable of synthesizing mature miRNA, as revealed by their loss of miR-30a. In contrast, expression of glomerular endothelial and mesangial cell miRNAs (miR-126 and miR-145, respectively) was unchanged. These findings demonstrate a critical role for miRNA in glomerular function and suggest a pathway that may participate in the pathogenesis of kidney diseases of podocyte origin. The unique architecture of podocytes may make them especially susceptible to cytoskeletal alterations initiated by aberrant miRNA dynamics.
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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.