ArticleJournal of molecular medicine (Berlin, Germany)2018
Inducible ATF3-NFAT axis aggravates podocyte injury.
Article in Journal of molecular medicine (Berlin, Germany), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 33 citations in OpenAlex.
- Transcriptome and weighted gene co-expression network analysis identify hub genes and pathways in rat kidneys after deep hypothermic circulatory arrest.Renal failure · 2026Article
- Integrated transcriptomic analysis of LMB2-induced podocyte injury identifies conserved inflammatory and adaptive stress responses.PloS one · 2026Article
- ST32da, a NovelCells · 2025Article
- Unlocking the therapeutic potential of the NFAT pathway in kidney diseases.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- The Dual Role and Therapeutic Implications of the Wnt/β-Catenin Pathway in Diabetic Kidney Disease.International journal of general medicine · 2025Review
- CaMKII may regulate renal tubular epithelial cell apoptosis through YAP/NFAT2 in acute kidney injury mice.Renal failure · 2023Article
- Anandamide modulates WNT-5A/BCL-2, IP3/NFATc1, and HMGB1/NF-κB trajectories to protect against mercuric chloride-induced acute kidney injury.Scientific reports · 2023Article
- ATF3/SPI1/SLC31A1 Signaling Promotes Cuproptosis Induced by Advanced Glycosylation End Products in Diabetic Myocardial Injury.International journal of molecular sciences · 2023Article
- Flot2 acts as a novel mediator of podocyte injury in proteinuric kidney disease.International journal of biological sciences · 2023Article
- Lipopolysaccharide-induced podocyte injury is regulated by calcineurin/NFAT and TLR4/MyD88/NF-κB signaling pathways through angiopoietin-like protein 4.Genes & diseases · 2022Article
- Integrated bioinformatics analysis reveals novel key biomarkers in diabetic nephropathy.SAGE open medicine · 2022Article
- Decoding the Mechanism behind the Pathogenesis of the Focal Segmental Glomerulosclerosis.Computational and mathematical methods in medicine · 2022Article
- Screening and Identification of Hub Genes in the Development of Early Diabetic Kidney Disease Based on Weighted Gene Co-Expression Network Analysis.Frontiers in endocrinology · 2022Article
- The complex role of Wnt ligands in type 2 diabetes mellitus and related complications.Journal of cellular and molecular medicine · 2021Review
- Role of NFAT in the Progression of Diabetic Atherosclerosis.Frontiers in cardiovascular medicine · 2021Review
- Identification of Hub Genes and Potential ceRNA Networks of Diabetic Nephropathy by Weighted Gene Co-Expression Network Analysis.Frontiers in genetics · 2021Article
- Identification of hub genes in diabetic kidney disease via multiple-microarray analysis.Annals of translational medicine · 2020Article
- [NFAT2 mediates high glucose-induced apoptosis in glomerular podocytesNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2018Article
- Astragaloside IV/lncRNA-TUG1/TRAF5 signaling pathway participates in podocyte apoptosis of diabetic nephropathy rats.Drug design, development and therapy · 2018Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Podocyte injury and loss contribute to proteinuria, glomerulosclerosis, and eventually kidney failure. Activating transcription factor 3 (ATF3) is a stress inducible transcription factor that is transiently expressed following stimulation. However, we show for the first time an induction of ATF3 in podocytes from patients with chronic kidney disease, including minimal change disease, focal segmental glomerulosclerosis, and diabetic nephropathy. The role of ATF3 induction in podocytes under chronic conditions is currently unknown. Compared with the control (C57 or BKS), ATF3 expression was elevated in animal model of proteinuria (LPS-treated C57 mice) and the model of diabetic nephropathy (db/db mice). Similarly, ATF3 was increased in high glucose (HG)-treated, lipopolysaccharide (LPS)-treated, or Ionomycin-treated podocytes in vitro. Overexpression of ATF3 increased podocyte apoptosis and decreased expression of podocin, the cell marker of podocyte; in contrast, ATF3-small interfering RNA knockdown reduced podocyte apoptosis and increased podocin expression. The translocation of ATF3 to the nucleus was increased upon stimulation. ATF3 directly modulates the regulation of NFATc1 gene promoter activity and alters the expression of Wnt6 and Fzd9, direct target genes of NFATc1 signaling. The ATF3 binding site of NFATc1 gene promoter is located at the region 671-775 base pairs upstream of the transcription start site. These results indicate a novel inducible axis of ATF3-NFAT in podocyte injury and loss. KEY MESSAGES: • The stress factor ATF3 is induced in podocytes from proteinuric patients, including diabetes. • ATF3 increased podocyte apoptosis and injury. • ATF3 directly modulates the regulation of NFATc1 gene promoter activity.
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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.