Identification of circRNA-miRNA-mRNA Regulatory Network and Autophagy Interaction Network in Atrial Fibrillation Based on Bioinformatics Analysis

Chao, Xiaoying; Dai, Weiran; Li, Shuo; Jiang, Chenyang; Jiang, Zhiyuan; Zhong, Guoqiang

doi:10.2147/ijgm.s333752

Cited by 3 publications

(2 citation statements)

References 52 publications

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“…In accordance with this hypothesis, a recent gene study showed an increased expression of 11 autophagy-related genes (CDKN1A, CXCR4, DIRAS3, HSP90AB1, ITGA3, PRKCD, TP53INP2, DAPK2, IFNG, PTK6, and TNFSF10) in AF [33]. In addition, the analysis of circular RNA (circRNA) to analyze differentially expressed circRNAs (DECs) identified a circRNA-miRNA-mRNA regulatory network consisting of 11 DECs, 9 target miRNAs, and 410 target genes [34]. These results suggest that autophagy may be implicated in the pathogenesis of AF.…”

Section: Discussionmentioning

confidence: 70%

Aging-Related Decline of Autophagy in Patients with Atrial Fibrillation—A Post Hoc Analysis of the ATHERO-AF Study

et al. 2022

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Background: Aging is an independent risk factor for cardiovascular diseases. The autophagy process may play a role in delaying aging and improving cardiovascular function in aging. Data regarding autophagy in atrial fibrillation (AF) patients are lacking. Methods: A post hoc analysis of the prospective ATHERO-AF cohort study, including 150 AF patients and 150 sex- and age-matched control subjects (CS), was performed. For the analysis, the population was divided into three age groups: <50–60, 61–70, and >70 years. Oxidative stress (Nox2 activity and hydrogen peroxide, H2O2), platelet activation (PA) by sP-selectin and CD40L, endothelial dysfunction (nitric oxide, NO), and autophagy parameters (P62 and ATG5 levels) were assessed. Results: Nox2 activity and H2O2 production were higher in the AF patients than in the CS; conversely, antioxidant capacity was decreased in the AF patients compared to the CS, as was NO production. Moreover, sP-selectin and CD40L were higher in the AF patients than in the CS. The autophagy process was also significantly impaired in the AF patients. We found a significant difference in oxidative stress, PA, NO production, and autophagy across the age groups. Autophagy markers correlated with oxidative stress, PA, and endothelial dysfunction in both groups. Conclusions: This study provides evidence that the autophagy process may represent a mechanism for increased cardiovascular risk in the AF population.

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Section: Discussionmentioning

confidence: 70%

Aging-Related Decline of Autophagy in Patients with Atrial Fibrillation—A Post Hoc Analysis of the ATHERO-AF Study

et al. 2022

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“…However, the speci c underlying mechanisms of these genes in AF require further clari cation. [24,25]. Our study indicates that hsa-miR-129-5p, hsa-miR-495-3p, hsa-miR-200c-3p, hsa-miR-92b-3p, and hsa-miR-429 are involved in the pathophysiological processes of atrial brillation (AF), suggesting their potential as targets for the prevention and treatment of AF.…”

Section: Disscusionmentioning

confidence: 89%

Identification and validation of oxidative stress-related genes in patients with atrial fibrillation

Dong,

Yan,

Zhang

et al. 2024

Preprint

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Background: Atrial fibrillation (AF) significantly elevates the risk of ischemic stroke.The upsurge in cardiovascular diseases associated with aging is, in part, attributed to oxidative stress.The objective of this research was to discover key genes associated with oxidative stress (OSGs) that could be used as biomarkers for diagnosing AF using bioinformatics analysis. Methods: Utilizing the AmiGO 2 database, cellular OSGs were identified.The AF patient datasets GSE115574 and GSE79768 were obtained from the Gene Expression Omnibus (GEO) database. GSE115574 was designated as the training set, while GSE79768 served as the validation set. Differentially expressed genes (DEGs) associated with AF were identified specifically from the GSE115574 dataset. DEOSGs resulted from the intersection of OSGs and DEGs, followed by bioinformatics analysis to determine hub genes. Potential diagnostic genes were identified through analyses of gene expression, ROC curves, and nomograms. The miRNA-diagnosis gene regulatory network was established. Finally, targeted drug predictions were conducted. Results: A total of 339 DEGs were identified from GSE115574, and 452 OSGs were obtained from the AmiGO 2 database. The intersection of DEGs and OSGs comprised 18 DEOSGs, including 12 oxidative stress-suppressor genes and 6 oxidative stress-inducible genes. Ten hub genes, namely JUN, ADIPOQ, AREG, COL1A1, FOS, IL6, KLF4, NR4A2, SOD2, and UCP2, were chosen. Additionally, five diagnostic genes—JUN, AREG, KLF4, SOD2, and UCP2—were identified. ROC analysis revealed the area under the curves (AUCs) of KLF4, JUN, UCP2, AREG, and SOD2 to be 0.733, 0.800, 0.760, 0.684, and 0.640 in the GSE115574 and 0.833, 0.786, 0.667, 0.952, and 0.786 in the GSE79768 dataset. Lastly, leveraging these five diagnostic genes, we identified potential drugs, such as 1,2-Dimethylhydrazine, for targeting oxidative stress-related AF treatment. Conclusion: The study findings suggest a significant involvement of OSGs in AF. JUN, AREG, KLF4, SOD2, and UCP2 emerge as potential specific biomarkers for early AF diagnosis and therapeutic targeting.

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Uncovering the Significance of JNK/AKT Axis in the Autophagic Regulation of Leishmania major Infection

Guhe,

Singh

2024

Molecular Microbiology

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The role of autophagy in host induced by infection of parasites of the Leishmania genus remains inadequately understood. Leishmania parasites modulate host macrophages to promote its survival by inducing autophagy response in the host cell. In this study, we conducted an investigation of L. major infection, focusing on host autophagy processes where we reconstructed two mathematical models elucidating autophagy induction and inhibition processes and its impact on parasite survival. Our models presented systems modulatory dynamics of the parasite‐mediated host autophagy. Our work highlighted the pivotal role of signaling molecules associated with the immune response which included signaling induced by Toll‐like receptor (TLR), specifically through regulation of JNK and AKT. Both molecules emerged as key regulators of host autophagy process, highlighting that JNK/AKT signaling axis may be a potential avenue for innovative therapeutic approaches in targeting leishmaniasis. Also, ATG16L complex was identified as a critical determinant in shaping the course of leishmanial infection through formation of autophagosomes. Through in vitro analyses in differentiated human monocyte cell line, we observed an increase in nitric oxide synthase (iNOS) concentration upon autophagy inhibition, while autophagy induction resulted in decreased iNOS concentration. This suggested that autophagy induction favors parasite survival in the host, potentially by providing a nutrient source that may be advantageous for the parasite. Inhibition of host autophagy promoted parasite elimination. Hence, our work proposed an avenue for strategically blocking host autophagy which enumerates a targeted approach for combating leishmaniasis.

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Identification of circRNA-miRNA-mRNA Regulatory Network and Autophagy Interaction Network in Atrial Fibrillation Based on Bioinformatics Analysis

Cited by 3 publications

References 52 publications

Aging-Related Decline of Autophagy in Patients with Atrial Fibrillation—A Post Hoc Analysis of the ATHERO-AF Study

Aging-Related Decline of Autophagy in Patients with Atrial Fibrillation—A Post Hoc Analysis of the ATHERO-AF Study

Identification and validation of oxidative stress-related genes in patients with atrial fibrillation

Uncovering the Significance of JNK/AKT Axis in the Autophagic Regulation of Leishmania major Infection

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