ArticleScientific reports2016
Role of C/EBP-α in Adriamycin-induced podocyte injury.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 25 citations in OpenAlex.
- Metabolic reprogramming, macrophage polarization, and intercellular crosstalk in pelvic inflammatory disease: emerging paradigms and therapeutic opportunities.Frontiers in immunology · 2026Review
- Cells of all trades - on the importance of spatial positioning of senescent cells in development, healing and aging.FEBS letters · 2025Review
- Adriamycin-induced nephropathy models: elucidating CKD pathophysiology and advancing therapeutic strategies.Experimental animals · 2025Review
- SA4503 Mitigates Adriamycin-Induced Nephropathy via Sigma-1 Receptor in Animal and Cell-Based Models.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Podocyte senescence: from molecular mechanisms to therapeutics.Renal failure · 2024Review
- ATP dynamics as a predictor of future podocyte structure and function after acute ischemic kidney injury in female mice.Nature communications · 2024Article
- C/EBPα-mediated ACSL4-dependent ferroptosis exacerbates tubular injury in diabetic kidney disease.Cell death discovery · 2024Article
- Pifithrin-α ameliorates glycerol induced rhabdomyolysis and acute kidney injury by reducing p53 activation.Renal failure · 2022Article
- CCAAT/Enhancer-Binding Proteins in Fibrosis: Complex Roles Beyond Conventional Understanding.Research (Washington, D.C.) · 2022Review
- ATDiabetologia · 2021Article
- A Personalized Glomerulus Chip Engineered from Stem Cell-Derived Epithelium and Vascular Endothelium.Micromachines · 2021Article
- Roles of Krüppel-like factor 5 in kidney disease.Journal of cellular and molecular medicine · 2021Review
- Mesenchymal Stem Cells Ameliorate Renal Inflammation in Adriamycin-induced Nephropathy.Immune network · 2019Article
- C/EBPα deficiency in podocytes aggravates podocyte senescence and kidney injury in aging mice.Cell death & disease · 2019Article
- Mature induced-pluripotent-stem-cell-derived human podocytes reconstitute kidney glomerular-capillary-wall function on a chip.Nature biomedical engineering · 2017Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Podocytes are terminally differentiated epithelial cells in the kidney glomeruli that act as a key component of the glomerular filtration barrier. Although the inciting injury to the podocyte may vary between various glomerular diseases, the inevitable consequence of podocyte injury results in their loss, leading to progressive kidney disease. Here, we report that the expression of CCAAT/enhancer binding protein-α (C/EBP-α), a transcription factor known to interact with and activate PPAR-γ and NF-κB, is suppressed in the glomerular cells, particularly in podocytes, in human kidneys with focal segmental glomerulosclerosis. Genetic ablation of C/EBP-α in podocytes resulted in increased proteinuria, increased podocyte foot process effacement, and to decreased podocyte number in the setting of Adriamycin (ADR)-induced nephropathy. Overexpression of C/EBP-α in human podocytes in vitro led to an inhibition of MCP-1 and IL-6 expression in response to TNF-α and IL-1β treatments. Conversely, augmented production of MCP-1 and IL-6 was observed in the glomeruli of C/EBP-α knockout mice and was associated increased infiltration of macrophages in vivo. Together, our data suggest that C/EBP-α mediates anti-inflammatory effects in podocytes to confer protection against podocyte injury and loss that may contribute to worsening glomerulosclerosis.
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Registered trials
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