ArticleJournal of the American Society of Nephrology : JASN2014
Overexpression of Mafb in podocytes protects against diabetic nephropathy.
Article in Journal of the American Society of Nephrology : JASN, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 39 citations in OpenAlex.
- MAFB Overexpression in Macrophages Promotes Wound Healing in Diabetic Foot Ulcer by Transcriptionally Activating WDR74 to Drive a Tissue-Repair Phenotype and Suppress Inflammation and Oxidative Stress.Applied biochemistry and biotechnology · 2026Article
- Astragaloside IV Alleviates Podocyte Injury in Diabetic Nephropathy through Regulating IRE-1α/NF-κ B/NLRP3 Pathway.Chinese journal of integrative medicine · 2025Article
- Expression of MAF bZIP transcription factor B protects against ulcerative colitis through the inhibition of the NF-κB pathway.Immunity, inflammation and disease · 2024Article
- MafB regulates NLRP3 inflammasome activation by sustaining p62 expression in macrophages.Communications biology · 2023Article
- An in vitro approach to understand contribution of kidney cells to human urinary extracellular vesicles.Journal of extracellular vesicles · 2023Article
- Podocyte-specific Transcription Factors: Could MafB Become a Therapeutic Target for Kidney Disease?Internal medicine (Tokyo, Japan) · 2023Review
- Article
- Preparation of single-cell suspensions of mouse glomeruli for high-throughput analysis.Nature protocols · 2021Review
- Oxidative Stress Genes in Diabetes Mellitus Type 2: Association with Diabetic Kidney Disease.Oxidative medicine and cellular longevity · 2021Article
- Sleeve Gastrectomy Attenuates Diabetic Nephropathy by Upregulating Nephrin Expressions in Diabetic Obese Rats.Obesity surgery · 2020Article
- Transcription factor 21 expression in injured podocytes of glomerular diseases.Scientific reports · 2020Article
- Effect of fosinopril on the renal cortex protein expression profile of Otsuka Long-Evans Tokushima Fatty rats.Experimental and therapeutic medicine · 2020Article
- Diabetic Nephropathy: Novel Molecular Mechanisms and Therapeutic Targets.Frontiers in pharmacology · 2020Review
- Neuron-specific Mafb knockout causes growth retardation accompanied by an impaired growth hormone/insulin-like growth factor I axis.Experimental animals · 2019Article
- LncRNA ZEB1-AS1 inhibits renal fibrosis in diabetic nephropathy by regulating the miR-217/MAFB axis.RSC advances · 2019Article
- Article
- Mice harboring an MCTO mutation exhibit renal failure resembling nephropathy in human patients.Experimental animals · 2019Article
- Erzhi Formula Extracts Reverse Renal Injury in Diabetic Nephropathy Rats by Protecting the Renal Podocytes.Evidence-based complementary and alternative medicine : eCAM · 2018Article
- MAFB mediates the therapeutic effect of sleeve gastrectomy for obese diabetes mellitus by activation of FXR expression.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2018Article
- Prolonged exposure of mouse and human podocytes to insulin induces insulin resistance through lysosomal and proteasomal degradation of the insulin receptor.Diabetologia · 2017Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We previously showed that the transcription factor Mafb is essential for podocyte differentiation and foot process formation. Podocytes are susceptible to injury in diabetes, and this injury leads to progression of diabetic nephropathy. In this study, we generated transgenic mice that overexpress Mafb in podocytes using the nephrin promoter/enhancer. To examine a potential pathogenetic role for Mafb in diabetic nephropathy, Mafb transgenic mice were treated with either streptozotocin or saline solution. Diabetic nephropathy was assessed by renal histology and biochemical analyses of urine and serum. Podocyte-specific overexpression of Mafb had no effect on body weight or blood glucose levels in either diabetic or control mice. Notably, albuminuria and changes in BUN levels and renal histology observed in diabetic wild-type animals were ameliorated in diabetic Mafb transgenic mice. Moreover, hyperglycemia-induced downregulation of Nephrin was mitigated in diabetic Mafb transgenic mice, and reporter assay results suggested that Mafb regulates Nephrin directly. Mafb transgenic glomeruli also overexpressed glutathione peroxidase, an antioxidative stress enzyme, and levels of the oxidative stress marker 8-hydroxydeoxyguanosine decreased in the urine of diabetic Mafb transgenic mice. Finally, Notch2 expression increased in diabetic glomeruli, and this effect was enhanced in diabetic Mafb transgenic glomeruli. These data indicate Mafb has a protective role in diabetic nephropathy through regulation of slit diaphragm proteins, antioxidative enzymes, and Notch pathways in podocytes and suggest that Mafb could be a therapeutic target.
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