ArticleEBioMedicine2019
FoxO1-mediated inhibition of STAT1 alleviates tubulointerstitial fibrosis and tubule apoptosis in diabetic kidney disease.
Article in EBioMedicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.
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Who cites it
71 citing papers in PubMed.
- Metabolic surgery mitigates early kidney injury in obese youth with diabetes by suppressing mTORC1/JAK/STAT signaling.The Journal of clinical investigation · 2026Trial
- Activation of the TGF-β1/HIPK2 signaling pathway exacerbates EMT injury in renal tubular epithelial cells in diabetic kidney disease.Renal failure · 2026Article
- GABA ameliorates diabetic kidney disease-induced podocyte injury via JAML-FPR2 axis-mediated suppression of macrophage infiltration.Renal failure · 2026Article
- Berberine attenuates diabetic kidney injury via FOXO1/SP1-associated regulation of renal SGLT-2 expression.Chinese medicine · 2026Article
- The AMPK/NRF2/FOXO Axis in CKD-Molecular and Clinical Perspectives.Antioxidants (Basel, Switzerland) · 2026Review
- HNF4A P2 isoform alleviates kidney fibrosis by inhibiting dedifferentiation of proximal tubular cells through JAG1/NOTCH signaling.Cellular & molecular biology letters · 2026Article
- Analysis of high glucose injury using human induced pluripotent stem cell-derived kidney organoids.BMC nephrology · 2026Article
- Tubular injury in diabetic kidney disease: a focus on regulated cell death.Frontiers in endocrinology · 2026Review
- CD248, targeted by veratramine and neobavaisoflavone, mediates pathological changes of renal tubular epithelial cells induced by high glucose.Hereditas · 2025Article
- Article
- PANoptosis: A novel therapeutic target in kidney disease (Review).International journal of molecular medicine · 2025Review
- Proteomics reveals the key transcription-related factors mediating obstructive nephropathy in pediatric patients and mice.Renal failure · 2025Article
- Mechanism ofRenal failure · 2025Article
- Circular RNA circDhx32 promotes cardiac inflammatory responses in mouse cardiac ischemia-reperfusion injury via binding to FOXO1 competed with AdipoR1.Acta pharmacologica Sinica · 2025Article
- Molecular Basis of Oxidative Stress-Induced Acute Kidney Injury, Kidney Fibrosis, Chronic Kidney Disease, and Clinical Significance of Targeting Reactive Oxygen Species-Regulated Pathways to Treat Kidney Disease.Frontiers in bioscience (Scholar edition) · 2025Review
- Finerenone Modulates PANoptosis to Improve Immune Microenvironment in Diabetic Nephropathy: A Machine Learning-Based Mechanistic Analysis.Journal of molecular neuroscience : MN · 2025Article
- Targeted Delivery of Triptolide Alleviates Diabetic Nephropathy via Inactivation of JAK2-STAT1 Signaling.Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2025Article
- Uncovering key markers and therapeutic targets for renal fibrosis in diabetic kidney disease through bulk and single-cell RNA sequencing.Journal of translational medicine · 2025Article
- Investigating the potential of oxidative stress-related gene as predictive markers in idiopathic pulmonary fibrosis.Scientific reports · 2025Article
- Ablation of macrophage transcriptional factor FoxO1 protects against ischemia-reperfusion injury-induced acute kidney injury.Acta pharmaceutica Sinica. B · 2025Article
11 more citing papers are in PubMed but not listed here.
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10 authors.
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Abstract
backgroundTubulointerstitial fibrosis (TIF) plays an important role in the progression of diabetic kidney disease (DKD). Forkhead box O1 (FoxO1) is involved in the regulation of metabolism and cell apoptosis, but its function in renal TIF induced by DKD is less well understood.
methodsHuman kidney biopsies with DKD and normal controls were used to detect apoptosis and TIF induced by diabetes. A mouse model with kidney-specific overexpression of Pax2-3aFoxO1 was established to further investigate the functions of FoxO1 in vivo. The in vitro roles of FoxO1 were analyzed in HK-2 cells with 3aFoxO1-knockin (3aFoxO1-KI) or FoxO1-knockdown (FoxO1-KD) via CRISPR/Cas9. Western blot, immunohistochemistry, and chromatin immunoprecipitation were used to explore the underlying mechanisms.
findingsIn this study, DKD patients had increased renal TIF and apoptosis. In vivo study showed that kidney-specific overexpression of Pax2-3aFoxO1 significantly reduced the expression of p-STAT1 with resultant renal functional impairment, retarding renal TIF and apoptosis in diabetic mice. Meanwhile, We observed that FoxO1-KD in HK-2 cells aggravated the expression of p-STAT1, leading to activation of epithelial-to-mesenchymal transition (EMT) and intrinsic apoptotic pathway. Conversely, EMT and apoptosis were significantly attenuated in HK-2 cells with 3aFoxO1-KI under hyperglycemic conditions.
interpretationTaken together, these data suggest that the protection role of FoxO1 against renal TIF and apoptosis in DKD is likely in part to target STAT1 signaling, which may be a promising strategy for long-term treatment of DKD. FUND: This work was supported by grants from the National Natural Science Foundation of China (grant numbers: 81570746 and 81770812).
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