High Glucose-Induced Human Kidney Cell Apoptosis and Inflammatory Injury Are Alleviated by Circ_0008529 Knockdown via Circ_0008529-Mediated miR-485-5p/WNT2B Signaling

Honghua, Lu

doi:10.1007/s12010-022-04088-z

Cited by 5 publications

(2 citation statements)

References 28 publications

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“…Wang et al 42 reported that miR‐218‐5p expressed in endothelial progenitor cells contributes to the development and repair of the kidney microvasculature. CirC_0008529/miR‐485‐5p/WNT2B was a vital signaling axis to regulate high glucose‐induced renal cell apoptosis and inflammatory injury 43 . The research of miR‐532‐5p uncovered that LINC00052 ameliorates acute kidney injury by sponging miR‐532‐5p and activating the Wnt signaling pathway 44 .…”

Section: Discussionmentioning

confidence: 99%

“…CirC_0008529/miR‐485‐5p/WNT2B was a vital signaling axis to regulate high glucose‐induced renal cell apoptosis and inflammatory injury. 43 The research of miR‐532‐5p uncovered that LINC00052 ameliorates acute kidney injury by sponging miR‐532‐5p and activating the Wnt signaling pathway. 44 miR‐6884‐5p regulates the functions of proliferation, invasion, epithelial–mesenchymal transformation in tumors; however, there are rarely research to reveal the function and mechanism of kidney diseases.…”

Section: Discussionmentioning

confidence: 99%

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Comprehensive analysis of fifteen hub genes to identify a promising diagnostic model, regulated networks, and immune cell infiltration in acute kidney injury

Sun

Cao

Huang

et al. 2022

Clinical Laboratory Analysis

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Background Acute kidney injury is a common clinical problem with no sensitive and specific diagnostic biomarkers and definitive treatments. The underlying molecular mechanisms of acute kidney injury are unclear. Therefore, it is pivotal to explore the underlying mechanisms and screen for novel diagnostic biomarkers, and therapeutic targets. Methods The present study identified 15 hub genes by WGCNA analysis. LASSO‐based logistic regression analysis was used to select key features and construct a diagnostic model of AKI. In addition, GO and KEGG analyses were performed and TF‐mRNA and miRNA‐mRNA network analysis and immune infiltration analysis of hub genes were performed to reveal the underlying mechanisms of AKI. Results A diagnostic model was constructed by LASSO‐based logistic regression analysis and was validated by RT‐qPCR based on 15 hub genes. GO and KEGG analyses revealed DEGs were enriched in oxidation–reduction process, cell adhesion, proliferation, migration, and metabolic process. The enriched TFs were BRD2, EP300, ETS1, MYC, SPI1, and ZNF263. The enriched miRNAs were miR‐181c‐5p, miR‐218‐5p, miR‐485‐5p, miR‐532‐5p and miR‐6884‐5p. The immune infiltration analysis showed that Macrophages M2 was decreasing significantly revealing a protective factor for further AKI treatment. Conclusions The present study identified 15 hub genes based on WGCNA. Development and validation of a potentially diagnostic model based on 15 hub genes. In addition, exploring the interaction between transcriptional factors and 15 hub genes, and miRNA‐mRNA relationship pairs. Furthermore, immune infiltration analysis was performed by analyzing gene expression profiles of AKI. Our study provides some basis for further experimental studies.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%