ArticleThe Korean journal of internal medicine2021
Role of Akt1 in renal fibrosis and tubular dedifferentiation during the progression of acute kidney injury to chronic kidney disease.
Article in The Korean journal of internal medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 27 citations in OpenAlex.
- A tri-scale in silico framework integrating pharmacovigilance and mechanistic modeling suggests tepotinib-associated acute kidney injury risk.Renal failure · 2026Article
- Integrative Network Pharmacology and Molecular Docking Analysis Uncovers Multi-Target Mechanisms of Alpha-Mangostin Against Acute Kidney Injury.Foods (Basel, Switzerland) · 2026Article
- Cell-state- and compartment-dependent PI3K/Akt redox signaling in chronic kidney disease: mechanisms and translational implications.Frontiers in pharmacology · 2026Review
- Role of the TGF‑β/Smad signaling pathway in the transition from acute kidney injury to chronic kidney disease (Review).International journal of molecular medicine · 2025Review
- Exploring the molecular mechanism of budesonide enteric capsules in the treatment of IgA nephropathy based on bioinformatics.Scientific reports · 2025Article
- Intermittent Fasting Protects Against the Progression from Acute Kidney Injury to Chronic Kidney Disease.Antioxidants (Basel, Switzerland) · 2025Article
- Investigation of the Potential Pharmacological Substance Basis and Mechanism of Action of Xuantu Granules in Treating Diabetic Kidney Disease Based on UHPLC-Q-Exactive-HRMS and Bioinformatics.Combinatorial chemistry & high throughput screening · 2025Article
- Targeting macrophage-myofibroblast transition withFrontiers in pharmacology · 2025Article
- Diosgenin Reduces Acute Kidney Injury and Ameliorates the Progression to Chronic Kidney Disease by Modifying the NOX4/p65 Signaling Pathways.Journal of agricultural and food chemistry · 2024Article
- Time-Restricted Feeding Protects against Renal Ischemia-Reperfusion Injury in Mice.International journal of molecular sciences · 2024Article
- Identification of inflammatory biomarkers in IgA nephropathy using the NanoString technology: a validation study in Caucasians.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- The effect ofTranslational andrology and urology · 2024Article
- Enteroendocrine cells and gut hormones as potential targets in the crossroad of the gut-kidney axis communication.Frontiers in pharmacology · 2023Review
- Chemokine (C-C Motif) Ligand 8 and Tubulo-Interstitial Injury in Chronic Kidney Disease.Cells · 2022Article
- Mechanisms of Qing-Gan Li-Shui Formulation in Ameliorating Primary Open Angle Glaucoma: An Analysis Based on Network Pharmacology.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Potential Molecular Mechanisms of Ephedra Herb in the Treatment of Nephrotic Syndrome Based on Network Pharmacology and Molecular Docking.BioMed research international · 2022Article
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Authors and funding
7 authors at 2 institutions in 1 country.
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Abstract
BACKGROUND/
aimsAcute kidney injury (AKI) is an underestimated yet important risk factor for the development of chronic kidney disease (CKD), characterized by tubulointerstitial fibrosis and tubular dedifferentiation. Tubular dedifferentiation, which is associated with the loss of epithelial markers and the gain of mesenchymal features, is thought to be involved in tubulointerstitial fibrosis. As protein kinase B/Akt is involved in the development of CKD, we investigated the role of Akt1, one of the three Akt isoforms, in a murine model of AKI-to-CKD progression.
methodsWe subjected C57BL/6 male mice to unilateral ischemia-reperfusion injury (UIRI) and harvested their kidneys after 6 weeks. Mice were divided into four groups, namely, wild-type (WT) UIRI, Akt1-/- UIRI, WT sham, and Akt1-/- sham.
resultsAkt1 (but not Akt2 or Akt3) was markedly activated in WT UIRI mice than in WT sham mice. Tubulointerstitial fibrosis and tubular dedifferentiation significantly increased in WT UIRI mice, but were attenuated in Akt1-/- UIRI mice. Both WT UIRI and Akt1-/- UIRI mice showed markedly upregulated transforming growth factor-β1 (TGF-β1)/Smad signaling compared with WT sham mice. However, TGF-β1/Smad expression did not differ between the two groups. The levels of phosphorylated GSK-3β, β-catenin, and Snail were attenuated in Akt1-/- UIRI mice compared with those in WT UIRI mice.
conclusionDeletion of Akt1 results in the attenuation of renal fibrosis and tubular dedifferentiation, independent of TGF-β1/Smad signaling, during AKI-to-CKD progression in a UIRI without contralateral nephrectomy model. Thus, Akt1 may serve as a therapeutic target in AKI-to-CKD progression.
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