Clinical Significance and Potential Mechanism of Circ_00008842 in Acute Myocardial Infarction

Zhang, Li; Wang, Ming; Liao, Ran; Han, Qing

doi:10.1536/ihj.24-009

Cited by 3 publications

References 40 publications

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miR-574-5p in epigenetic regulation and Toll-like receptor signaling

Yang

2024

Cell Commun Signal

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miR-574-5p is an unusual microRNA (miRNA) that is often upregulated or downregulated following exposure to irradiation or toxic chemicals; bacterial, parasitic or viral infection; and a variety of other disease conditions. Canonically, miR-574-5p epigenetically regulates the expression of many messenger RNAs (mRNAs) through miRNA-mediated posttranscriptional regulation, thereby affecting cellular physiology or pathophysiology and contributing to the pathogenesis or progression of a variety of diseases. However, recent studies have established that in addition to serving as a fine-tuning repressor of gene expression, miR-574-5p also stimulates gene expression as an endogenous ligand for Toll-like receptor-8/7 (TLR8/7). Indeed, the binding of miR-574-5p to TLR8/7 triggers the TLR signaling pathway, leading to the induction of interferons, inflammatory cytokines and autoimmune signaling. These findings suggest that miR-574-5p is not only an important epigenetic regulator of gene expression, but also an important regulator of immune and inflammatory responses. Abnormal miR-574-5p-TLR8/7 signaling has been shown to be tightly associated with inflammation-related cancers and a number of autoimmune disorders. miR-574-5p can serve as a potential biomarker for many diseases. Most importantly, miR-574-5p is a promising therapeutic target for the treatment or prevention of human disorders, especially infectious diseases, cancers and autoimmune diseases.

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miR-574-5p in epigenetic regulation and Toll-like receptor signaling

Yang

2024

Cell Commun Signal

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Ispinesib Mesylate-induced oxidative stress via miR-30e-5p/BCL2L11 axis in acute myocardial infarction: a comprehensive bioinformatics and experimental validation investigation

Ningxia,

Fei

2024

Preprint

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Objective Cardiovascular disorders constitute a substantial threat to global human health and safety. Of note, acute myocardial infarction (AMI), being a grave cardiovascular disorder, has garnered considerable attention owing to its elevated prevalence, mortality and broad demographic distribution. It is well established that hypoxia-induced apoptosis significantly contributes towards the onset and progression of AMI; however, several aspects regarding the biological indicators and molecular mechanisms of AMI remain elusive. Method This investigation utilized the Gene Expression Comprehensive (GEO) database to perform comprehensive analysis of pivotal genes employing techniques like differential analysis, Venn analysis, and weighted correlation network analysis (WGCNA). Subsequently, the correlation between the key genes and correlation factors was scrutinized, and the potential causal link between these factors and the outcome of AMI was probed via Mendelian randomization (MR). Additionally, real-time quantitative polymerase chain reaction (RT-qPCR) and lentivirus transfection experiments were executed, miRNA-mRNA networks were constructed utilizing miRBase databases, three-dimensional structures were predicted with the aid of RNAfold and Vfold3D databases, and drug sensitivity analysis was conducted using RNAactDrug databases. Result Following classification, WGCNA clustering, and Wien screening analysis, two distinctly expressed genes intimately linked to apoptosis - PTEN and BCL2L11 - were successfully identified. The outcomes of RT-qPCR and lentivirus infection experiments corroborated that the expression pattern of BCL2L11 conformed with our prior findings. Mendelian randomization analysis unveiled a robust causal relationship between BCL2L11 single nucleotide polymorphisms (SNPs) and AMI. Lastly, through miRNA-mRNA network and drug susceptibility analysis, it was discerned that the Ispinesib Mesylate, Bleomycin (50 uM)/miR-141-3p/BCL2L11 axis could potentially serve as efficacious therapeutic or preventive strategies against AMI. Conclusion In this study, we introduced the novel concepts of Ispinesib Mesylate and Bleomycin (50 uM)/miR-141-3p/BCL2L11 axis, offering a fresh perspective on the apoptotic mechanism in AMI.

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Methylophiopogonanone A Inhibits Ferroptosis in H9c2 Cells: An Experimental and Molecular Simulation Study

Wang,

Zhao,

Chen

et al. 2024

Molecules

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In this study, homoisoflavone methylophiopogonanone A (MOA) was investigated for its inhibitory effect on ferroptosis of H9c2 cells using a set of cellular assays, such as BODIPY-probed and H2DCFDA-probed flow cytometry analyses, cell counting kit-8 analysis (CCK-8), and lactate dehydrogenase (LDH) release analysis. All these cellular assays adopted Fer-1 as the positive control. Subsequently, MOA and Fer-1 were subjected to two antioxidant assays, i.e., 2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl 3-oxide radical (PTIO•)-scavenging and 2,2′-azinobis(3-ethylbenzo-thiazoline-6-sulfonic acid radical (ABTS•+)-scavenging. Finally, MOA, along with Fer-1, were systematically analyzed for molecular docking and dynamics simulations using a set of software tools. The experimental results revealed that MOA could inhibit ferroptosis of H9c2 cells but did not effectively scavenge PTIO• and ABTS•+ free radicals. Two molecular simulation methods or algorithms suggested that MOA possessed similar binding affinity and binding free energy (∆Gbind) to Fer-1. Visual analyses indicated various hydrophobic interactions between MOA and one of the seven enzymes, including superoxide dismutase (SOD), dihydroorotate dehydrogenase (DHODH), ferroportin1 (FPN), ferroptosis suppressor protein 1 (FSP1), glutathione peroxidase 4 (GPX4), nicotinamide adenine dinucleotide phosphate (NADPH), and solute carrier family 7 member 11 (SLC7A11). Based on these experimental and molecular simulation results, it is concluded that MOA, a homoisoflavonoid with meta-di-OHs, can inhibit ferroptosis in H9c2 cells. Its inhibitory effect is mainly attributed to the regulation of enzymes rather than direct free radical scavenging. The regulation of enzymes primarily depends on hydrophobic interactions rather than H-bond formation. During the process, flexibility around position 9 allows MOA to adjust to the enzyme binding site. All these findings provide foundational information for developing MOA and its derivatives as potential drugs for myocardial diseases.

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Clinical Significance and Potential Mechanism of Circ_00008842 in Acute Myocardial Infarction

Cited by 3 publications

References 40 publications

miR-574-5p in epigenetic regulation and Toll-like receptor signaling

miR-574-5p in epigenetic regulation and Toll-like receptor signaling

Ispinesib Mesylate-induced oxidative stress via miR-30e-5p/BCL2L11 axis in acute myocardial infarction: a comprehensive bioinformatics and experimental validation investigation

Methylophiopogonanone A Inhibits Ferroptosis in H9c2 Cells: An Experimental and Molecular Simulation Study

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