ArticleExperimental & molecular medicine2024
EPRS1-mediated fibroblast activation and mitochondrial dysfunction promote kidney fibrosis.
Article in Experimental & molecular medicine, 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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Who cites it
4 citing papers in PubMed.
- The Extracellular Matrix and the Immune System in Acute Lung Injury: Partners in Damage and Repair.Biomedicines · 2025Review
- Gut microbiota as a predictive tool for outcomes in IgA nephropathy.Renal failure · 2025Article
- Identification of actin cytoskeleton organization genes in oral cancer and oral potentially malignant disorders using oral tissue RNA-seq database.Medicina oral, patologia oral y cirugia bucal · 2025Article
- Autophagy-senescence interplay in kidney disease: mechanistic insights and therapeutic potential.Molecular biology reports · 2025Review
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Authors and funding
21 authors.
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Abstract
Kidney fibrosis causes irreversible structural damage in chronic kidney disease and is characterized by aberrant extracellular matrix (ECM) accumulation. Although glutamyl-prolyl-tRNA synthetase 1 (EPRS1) is a crucial enzyme involved in proline-rich protein synthesis, its role in kidney fibrosis remains unclear. The present study revealed that EPRS1 expression levels were increased in the fibrotic kidneys of patients and mice, especially in fibroblasts and proximal tubular epithelial cells, on the basis of single-cell analysis and immunostaining of fibrotic kidneys. Moreover, C57BL/6 EPRS1
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