ReviewCurrent opinion in nephrology and hypertension2020
Molecular regulation and function of FoxO3 in chronic kidney disease.
Review in Current opinion in nephrology and hypertension, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
14 citing papers in PubMed, 21 citations in OpenAlex.
- Metabolic surgery mitigates early kidney injury in obese youth with diabetes by suppressing mTORC1/JAK/STAT signaling.The Journal of clinical investigation · 2026Trial
- The AMPK/NRF2/FOXO Axis in CKD-Molecular and Clinical Perspectives.Antioxidants (Basel, Switzerland) · 2026Review
- Exploring plasma microRNA profiling and signaling pathways in comorbidity-free sickle cell anemia: a pilot case-control study.BMC research notes · 2026Article
- Molecular mechanism of propofol in reducing kidney injury induced by autologous orthotopic liver transplantation.Frontiers in immunology · 2026Article
- The effect of regular physical activity during hemodialysis on levels of FOXO proteins and myostatin concentration.Archives of medical science : AMS · 2026Article
- The differential expression of circulating microRNAs in sickle cell trait compared with the normal hemoglobin phenotype.Blood advances · 2025Article
- Transcriptomic Profiling of Hypoxia-Adaptive Responses in Tibetan Goat Fibroblasts.Animals : an open access journal from MDPI · 2025Article
- FoxO3 and oxidative stress: a multifaceted role in cellular adaptation.Journal of molecular medicine (Berlin, Germany) · 2023Review
- Ketogenic Diet and Ketone Bodies against Ischemic Injury: Targets, Mechanisms, and Therapeutic Potential.International journal of molecular sciences · 2023Review
- miR-122-5p Regulates Renal Fibrosis In Vivo.International journal of molecular sciences · 2022Article
- Energy Homeostasis Gene Nucleotide Variants and Survival of Hemodialysis Patients-A Genetic Cohort Study.Journal of clinical medicine · 2022Article
- Metformin Inhibits HaCaT Cell Proliferation Under Hyperlipidemia Through Reducing Reactive Oxygen Species via FOXO3 Activation.Clinical, cosmetic and investigational dermatology · 2022Article
- Suppression ofBiomolecules & therapeutics · 2021Article
- Longevity Factor FOXO3: A Key Regulator in Aging-Related Vascular Diseases.Frontiers in cardiovascular medicine · 2021Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
purpose of reviewFOXOs are transcription factors that regulate downstream target genes to counteract to cell stress. Here we review the function and regulation of FOXO transcription factors, the mechanism of FOXO3 activation in the kidney, and the role of FOXO3 in delaying the development of chronic kidney disease (CKD). RECENT
findingsProgressive renal hypoxia from vascular dropout and metabolic perturbation is a pathogenic factor for the initiation and development of CKD. Hypoxia and low levels of α-ketoglutarate generated from the TCA cycle inhibit prolyl hydroxylase domain (PHD)-mediated prolyl hydroxylation of FoxO3, thus reducing FoxO3 protein degradation via the ubiquitin proteasomal pathway, similar to HIF stabilization under hypoxic conditions. FoxO3 accumulation and nuclear translocation activate two key cellular defense mechanisms, autophagy and antioxidative response in renal tubular cells, to reduce cell injury and promote cell survival. FoxO3 directly activates the expression of Atg proteins, which replenishes core components of the autophagic machinery to allow sustained autophagy in the chronically hypoxic kidney. FoxO3 protects mitochondria by stimulating the expression of superoxide dismutase 2 (SOD2), as tubular deletion of FoxO3 in mice results in reduced SOD2 levels and profound mitochondrial damage. SUMMARY: Knowledge gained from animal studies may help understand the function of stress responsive transcription factors that could be targeted to prevent or treat CKD.
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Registered trials
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