FOXO1 inhibition prevents renal ischemia–reperfusion injury via cAMP‐response element binding protein/PPAR‐γ coactivator‐1α‐mediated mitochondrial biogenesis

Wang, Di; Wang, Yanqing; Zou, Xiantong; Shi, Yundi; Liu, Qian; Huyan, Tianru; Su, Jing; Wang, Qi; Zhang, Fengxue; Li, Xuejun; Tie, Lu

doi:10.1111/bph.14878

Cited by 69 publications

(42 citation statements)

References 62 publications

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“…The transcription factor Foxo1 is a “nutrient-sensor”. Depending upon the cellular stress levels, it shuttles between nucleus and mitochondria and binds to mitochondrial DNA (mtDNA) to regulate mitochondrial biogenesis and function [30, 31, 32]. Thus, reduced Foxo1 expression in Foxp1 +/– mice suggests that impaired mitochondrial biogenesis and function might play a role in the developmental defect of the Foxp1 +/− striatum [31, 32].…”

Section: Resultsmentioning

confidence: 99%

Mitochondrial dysfunction and oxidative stress contribute to cognitive and motor impairment in FOXP1 syndrome

Wang

Froehlich

Torres

et al. 2021

Preprint

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There is increasing evidence that mitochondrial homeostasis - influenced by both genetic and environmental factors - is crucial in neurodevelopment. FOXP1 syndrome is a neurodevelopmental disorder that manifests motor dysfunction, intellectual disability, autism and language impairment. In this study, we used a Foxp1+/- mouse model to address whether cognitive and motor deficits in FOXP1 syndrome are associated with mitochondrial dysfunction and oxidative stress. Here we show that genes with a role in mitochondrial biogenesis and dynamics (e.g. Foxo1, Pgc-1α, Tfam, Opa1, and Drp1) were dysregulated in the striatum of Foxp1+/- mice at different postnatal stages. Furthermore, in the striatum of Foxp1+/- animals, mitochondrial membrane potential was disrupted, and reactive oxygen species, lipid peroxidation and cytochrome c release were significantly elevated. These features can explain the reduced neurite branching, learning and memory, endurance, and motor coordination that we observed in these animals. Taken together, we provide strong evidence of mitochondrial dysfunction in Foxp1+/- mice, suggesting that insufficient energy supply and excessive oxidative stress underlies the cognitive and motor impairment in FOXP1 deficiency.

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Section: Resultsmentioning

confidence: 99%

Mitochondrial dysfunction and oxidative stress contribute to cognitive and motor impairment in FOXP1 syndrome

Wang

Froehlich

Torres

et al. 2021

Preprint

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“…The relationship between YTHDF1 expression and immune checkpoint (ICP) genes, biomarkers and ESTIMATE score in the TME was explored via the SangerBox website (http:// sangerbox.com/Tool), which is a useful online platform for TCGA data analysis (25). Immune checkpoint (ICP) genes were selected according to a previous study (26).…”

Section: Database Used To Analyze the Correlation Between Ythdf1 Expression And Immune Checkpoint (Icp) Genes Tumor Mutational Burden (Tmmentioning

confidence: 99%

YTHDF1 Is a Potential Pan-Cancer Biomarker for Prognosis and Immunotherapy

Qiu

et al. 2021

Front. Oncol.

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BackgroundYTH N6-methyladenosine RNA binding protein 1 (YTHDF1) has been indicated proven to participate in the cross-presentation of tumor antigens in dendritic cells and the cross-priming of CD8+ T cells. However, the role of YTHDF1 in prognosis and immunology in human cancers remains largely unknown.MethodsAll original data were downloaded from TCGA and GEO databases and integrated via R 3.2.2. YTHDF1 expression was explored with the Oncomine, TIMER, GEPIA, and BioGPS databases. The effect of YTHDF1 on prognosis was analyzed via GEPIA, Kaplan-Meier plotter, and the PrognoScan database. The TISIDB database was used to determine YTHDF1 expression in different immune and molecular subtypes of human cancers. The correlations between YTHDF1 expression and immune checkpoints (ICP), tumor mutational burden (TMB), microsatellite instability (MSI), and neoantigens in human cancers were analyzed via the SangerBox database. The relationships between YTHDF1 expression and tumor-infiltrated immune cells were analyzed via the TIMER and GEPIA databases. The relationships between YTHDF1 and marker genes of tumor-infiltrated immune cells in urogenital cancers were analyzed for confirmation. The genomic alterations of YTHDF1 were investigated with the c-BioPortal database. The differential expression of YTHDF1 in urogenital cancers with different clinical characteristics was analyzed with the UALCAN database. YTHDF1 coexpression networks were studied by the LinkedOmics database.ResultsIn general, YTHDF1 expression was higher in tumors than in paired normal tissue in human cancers. YTHDF1 expression had strong relationships with prognosis, ICP, TMB, MSI, and neoantigens. YTHDF1 plays an essential role in the tumor microenvironment (TME) and participates in immune regulation. Furthermore, significant strong correlations between YTHDF1 expression and tumor immune-infiltrated cells (TILs) existed in human cancers, and marker genes of TILs were significantly related to YTHDF expression in urogenital cancers. TYHDF1 coexpression networks mostly participated in the regulation of immune response and antigen processing and presentation.ConclusionYTHDF1 may serve as a potential prognostic and immunological pan-cancer biomarker. Moreover, YTHDF1 could be a novel target for tumor immunotherapy.

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“…5 In our current FoxO1 and its downstream targets play a key role in mitochondrial biogenesis. [49][50][51] Transient insulin stimulation activates the PI3K-AKT signalling pathway and suppresses FoxO1 activation.…”

Section: Discussionmentioning

confidence: 99%

Kir6.1 improves cardiac dysfunction in diabetic cardiomyopathy via the AKT‐FoxO1 signalling pathway

Bai

Duan²,

Wang

et al. 2021

J Cellular Molecular Medi

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Diabetic cardiomyopathy (DCM), characterized by structural, morphological, functional and metabolic abnormalities in the heart, severely impairs the health of diabetic patients and often occurs independently of myocardial ischaemia, congenital heart disease, hypertension and other cardiovascular diseases. Numerous molecular mechanisms have been proposed to contribute to the development of DCM, including altered myocardial insulin signalling, mitochondrial dysfunction, increased oxidative stress, autophagy and dysregulation of Ca 2+ handling, 1 which result in cardiomyocyte necrosis, cardiac remodelling and both diastolic and systolic dysfunction. Among these, altered myocardial insulin signalling may be the most common feature linking diabetes-induced alterations to the development of cardiac dysfunction. 2 Our previous studies have found that prolonged high-fat diet (HFD) feeding of animal models impairs protein kinase B (AKT) activation and forkhead box protein O1 (FoxO1) transcription factor phosphorylation,

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FOXO1 inhibition prevents renal ischemia–reperfusion injury via cAMP‐response element binding protein/PPAR‐γ coactivator‐1α‐mediated mitochondrial biogenesis

Cited by 69 publications

References 62 publications

Mitochondrial dysfunction and oxidative stress contribute to cognitive and motor impairment in FOXP1 syndrome

Mitochondrial dysfunction and oxidative stress contribute to cognitive and motor impairment in FOXP1 syndrome

YTHDF1 Is a Potential Pan-Cancer Biomarker for Prognosis and Immunotherapy

Kir6.1 improves cardiac dysfunction in diabetic cardiomyopathy via the AKT‐FoxO1 signalling pathway

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