ArticleJournal of toxicologic pathology2024
CD44 expression in renal tubular epithelial cells in the kidneys of rats with cyclosporine-induced chronic kidney disease.
Article in Journal of toxicologic pathology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Predictive value of CD44 in membranous nephropathy with focal segmental glomerular sclerosis lesions treated with calcineurin inhibitors.Renal failure · 2026Article
- Kidney-targeted drug delivery: from physiological mechanisms to precision therapeutics.Frontiers in bioengineering and biotechnology · 2026Review
- Multimodal spatial transcriptomic characterization of mouse kidney injury and repair.Nature communications · 2025Article
- Single-cell transcriptomics reveals metabolic remodeling and functional specialization in the immune microenvironment of bone tumors.Journal of translational medicine · 2025Article
- Cyclosporine A Decreased Paclitaxel Resistance in Prostate Cancer Cells by Inhibiting MTDH Expression.American journal of men's healthArticle
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Authors and funding
5 authors.
Funding
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Abstract
Renal tubular epithelial cell (TEC) injury is the most common cause of drug-induced kidney injury (DIKI). Although TEC regeneration facilitates renal function and structural recovery following DIKI, maladaptive repair of TECs leads to irreversible fibrosis, resulting in chronic kidney disease (CKD). CD44 is specifically expressed in TECs during maladaptive repair in several types of rat CKD models. In this study, we investigated CD44 expression and its role in renal fibrogenesis in a cyclosporine (CyA) rat model of CKD. Seven-week-old male Sprague-Dawley rats fed a low-salt diet were subcutaneously administered CyA (0, 15, or 30 mg/kg) for 28 days. CD44 was expressed in atrophic, dilated, and hypertrophic TECs in the fibrotic lesions of the CyA groups. These TECs were collected by laser microdissection and evaluated by microarray analysis. Gene ontology analysis suggested that these TECs have a mesenchymal phenotype, and pathway analysis identified CD44 as an upstream regulator of fibrosis-related genes, including fibronectin 1 (
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