ArticleCurrent research in toxicology2024
The upregulation of lamin A/C as a compensatory mechanism during tight junction disruption in renal tubular cells mediated by calcium oxalate crystals.
Article in Current research in toxicology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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
4 citing papers in PubMed, 4 citations in OpenAlex.
- Transforming destructive mechanical cues into therapeutic power: Activation of PIEZO1 and TRPV4 counteracts mechano-induced damage of cellular junctions in Hailey-Hailey disease.Journal of advanced research · 2026Article
- Lactobacillus acidophilus abolishes oxalate-mediated renal epithelial barrier disruption and calcium oxalate monohydrate crystal adhesion to renal epithelial cells.Cellular & molecular biology letters · 2026Article
- Mechanical-biochemical signaling accelerates scleral remodeling in myopia via the LaminA/C-Emerin-MKL1 axis.Cell communication and signaling : CCS · 2026Article
- Advances in the mechanism of urinary proteins in calcium oxalate kidney stone formation.Urolithiasis · 2025Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Calcium oxalate monohydrate (COM), the most important crystal causing kidney stone disease, upregulates lamin A/C but downregulates zonula occludens-1 (ZO-1) in renal tubular cells. While roles for F-actin and α-tubulin and their association with ZO-1 are known to regulate COM-mediated tight junction (TJ) disruption, roles of lamin A/C and its interplay with ZO-1 in COM kidney stone model remain unclear and are thus the objectives of this study. Lamin A/C was knocked down in MDCK cells by silencing RNA specific for
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