ArticleThe Journal of clinical investigation2021
DACH1 protects podocytes from experimental diabetic injury and modulates PTIP-H3K4Me3 activity.
Article in The Journal of clinical investigation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- Approach to Studies on Podocyte Lesions Mediated by Hyperglycemia: A Systematic Review.International journal of molecular sciences · 2025Pooled it
- Trained immunity: New insights into pathogenesis and therapeutic targets in diabetes and diabetic complications.Genes & diseases · 2026Review
- Beyond hyperglycemia: histone modification-mediated epigenetic dysregulation in diabetic retinopathy and nephropathy.Diabetology & metabolic syndrome · 2026Review
- PTIP inhibits proliferation, migration, and angiogenesis of retinal microvascular endothelial cells in a high-glucose environment.In vitro cellular & developmental biology. Animal · 2026Article
- Chromatin remodeling and epigenetic regulation in chronic kidney disease.Frontiers in genetics · 2026Review
- Role of nuclear receptors, lipid metabolism, and mitochondrial function in the pathogenesis of diabetic kidney disease.American journal of physiology. Renal physiology · 2025Review
- Curcumin targets CXCL16-mediated podocyte injury and lipid accumulation in diabetic kidney disease treatment.Archives of pharmacal research · 2024Article
- Histone methylation modification and diabetic kidney disease: Potential molecular mechanisms and therapeutic approaches (Review).International journal of molecular medicine · 2024Review
- DACH1 attenuated PA-induced renal tubular injury through TLR4/MyD88/NF-κB and TGF-β/Smad signalling pathway.Journal of endocrinological investigation · 2024Article
- A simple protocol to establish a conditionally immortalized mouse podocyte cell line.Scientific reports · 2024Article
- Nucleic acid and protein methylation modification in renal diseases.Acta pharmacologica Sinica · 2024Review
- MiR-29b Alleviates High Glucose-induced Inflammation and Apoptosis in Podocytes by Down-regulating PRKAB2.Endocrine, metabolic & immune disorders drug targets · 2024Article
- Study on Potential Differentially Expressed Genes in Idiopathic Pulmonary Fibrosis by Bioinformatics and Next-Generation Sequencing Data Analysis.Biomedicines · 2023Article
- Retinal determination gene networks: from biological functions to therapeutic strategies.Biomarker research · 2023Review
- Functioning and mechanisms of PTMs in renal diseases.Frontiers in pharmacology · 2023Review
- Epigenetic modification in diabetic kidney disease.Frontiers in endocrinology · 2023Review
- An integrated co-expression network analysis reveals novel genetic biomarkers for immune cell infiltration in chronic kidney disease.Frontiers in immunology · 2023Article
- Network-based identification and prioritization of key transcriptional factors of diabetic kidney disease.Computational and structural biotechnology journal · 2023Article
- Podocyte-specific Transcription Factors: Could MafB Become a Therapeutic Target for Kidney Disease?Internal medicine (Tokyo, Japan) · 2023Review
- Zuogui Wan ameliorates high glucose-induced podocyte apoptosis and improves diabetic nephropathy in db/db mice.Frontiers in pharmacology · 2022Article
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24 authors at 6 institutions in 2 countries.
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Abstract
Dachshund homolog 1 (DACH1), a key cell-fate determinant, regulates transcription by DNA sequence-specific binding. We identified diminished Dach1 expression in a large-scale screen for mutations that convert injury-resistant podocytes into injury-susceptible podocytes. In diabetic kidney disease (DKD) patients, podocyte DACH1 expression levels are diminished, a condition that strongly correlates with poor clinical outcomes. Global Dach1 KO mice manifest renal hypoplasia and die perinatally. Podocyte-specific Dach1 KO mice, however, maintain normal glomerular architecture at baseline, but rapidly exhibit podocyte injury after diabetes onset. Furthermore, podocyte-specific augmentation of DACH1 expression in mice protects from DKD. Combined RNA sequencing and in silico promoter analysis reveal conversely overlapping glomerular transcriptomic signatures between podocyte-specific Dach1 and Pax transactivation-domain interacting protein (Ptip) KO mice, with upregulated genes possessing higher-than-expected numbers of promoter Dach1-binding sites. PTIP, an essential component of the activating histone H3 lysine 4 trimethylation (H3K4Me3) complex, interacts with DACH1 and is recruited by DACH1 to its promoter-binding sites. DACH1-PTIP recruitment represses transcription and reduces promoter H3K4Me3 levels. DACH1 knockdown in podocytes combined with hyperglycemia triggers target gene upregulation and increases promoter H3K4Me3. These findings reveal that in DKD, diminished DACH1 expression enhances podocyte injury vulnerability via epigenetic derepression of its target genes.
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