UTP14A, DKC1, DDX10, PinX1, and ESF1 Modulate Cardiac Angiogenesis Leading to Obesity-Induced Cardiac Injury

Pan, Xiaoyu; Chen, Shuchun; Chen, Xing; Ren, Qingjuan; Yue, Lin; Niu, Shu; Li, Zelin; Zhu, Ruiyi; Chen, Xiaoyi; Jia, Zhuoya; Zhen, Ruoxi; Ban, Jiangli

doi:10.1155/2022/2923291

Cited by 10 publications

(4 citation statements)

References 40 publications

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“…Studies have found that CEACAM1 [237], STAT1 [238], ARG1 [239], TLR4 [240], LRRK2 [241], ABCA1 [242], PTGS2 [243], CYP2D6 [244], JAK2 [245], TLR2 [246], DUSP6 [247], CYP1B1 [248], CCR1 [249], HDAC9 [250], LATS2 [251], IL1RN [252], GCH1 [253], PELI1 [254], EGR1 [255], HIPK3 [256], CCR2 [257], GCLC (glutamate-cysteine ligase catalytic subunit) [258], KLF3 [259], VEGFA (vascular endothelial growth factor A) [260], ITGB1 [261], RASA1 [262], PTPN12 [263], SNRK (SNF related kinase) [264], PRKAR1A [265], LDLR (low density lipoprotein receptor) [266], SIRT1 [267], NOD2 [268], VCAN (versican) [269], TET2 [270], PFKFB2 [271], ZBTB20 [272], MYBL2 [273], PF4 [274], VEGFB (vascular endothelial growth factor B) [275], CCR7 [276], PRDX2 [277], HSPB1 [278], ZNF791 [279], IGFBP4 [280], ESF1 [281], SNHG8 [282], LGALS3 [283] and LGMN (legumain) [284] are altered expression in myocardial infarction. Altered expression of CEACAM1 [176], ACSL1 [285], STAT1 [286], TLR4 [287], ABCA1 [288], TLR5 [183], F2RL1 [289], CYP2D6 [290], PDK4 [291], RNF213 [186], JAK2 [292], TLR8 [189], NOTCH2 [293], CENPJ (centromere protein J) [294], FNIP1 [295], TLR2 [296], KIDINS220 [297], DUSP6 [298], CYP1B1 [299], S1PR3 [300], NCOA2 [301], HDAC9 [302], PELI1 [303], EGR1 [304], HIF1A [305], CCR2 [306], IR...…”

Section: Discussionmentioning

confidence: 99%

Identification of novel prognostic targets in coronary artery disease and related complications using bioinformatics and next generation sequencing data analysis

Vastrad¹,

Vastrad²

2023

Preprint

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Coronary artery disease (CAD) is the most common cardiovascular disorder and the leading cause of heart related deaths in world. Increasing molecular targets have been discovered for CAD and CAD - related complications prognosis and therapy. However, there is still an urgent need to identify novel biomarkers. Therefore, we evaluated biomarkers that might help the diagnosis and treatment of CAD and CAD related complications. We searched next generation sequencing (NGS) dataset (GSE202625) and identified differentially expressed genes (DEGs) by comparing CAD and normal control samples using DESeq2. Gene ontology (GO) and pathway enrichment analyses of the DEGs were performed using the g:Profiler online database. The protein protein interaction (PPI) network was plotted with IMEx interactome and visualized using Cytoscape. Module analysis of the PPI network was done using PEWCC1. MiRNA hub gene regulatory network and TF hub gene regulatory network analysis was performed to identify the hub genes, miRNAs and TFs. Receiver operating characteristic (ROC) curve analysis was used to predict the diagnostic effectiveness of the hub genes. A total of 118 DEGs (479 up regulated genes and 479 down regulated genes) were detected. The GO enrichment analysis indicated that the DEGs most significantly enriched in cellular response to stimulus and biosynthetic process. The REACTOME pathway enrichment analysis revealed that the DEGs were most significantly enriched in immune system and eukaryotic translation elongation. PPI network, modules, miRNA hub gene regulatory network and TF hub gene regulatory network analysis demonstrated that EGR1, SIRT1, STAT1, LRRK2, HIF1A, CSNK2B, RPS3, RPS2, RPS4X and HDAC11 were the hub genes. On the whole, the findings of this study enhance our understanding of the potential molecular mechanisms of CAD and CAD-related complications, and provide potential targets for further research.

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Section: Discussionmentioning

confidence: 99%

Identification of novel prognostic targets in coronary artery disease and related complications using bioinformatics and next generation sequencing data analysis

Vastrad¹,

Vastrad²

2023

Preprint

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“…Bioinformatics methods were executed following previous literature. 31 Diabetes, Metabolic Syndrome and Obesity 2024:17…”

Section: Screening Of Differentially Expressed Proteins (Deps)mentioning

confidence: 99%

Effect of Semaglutide and Empagliflozin on Pulmonary Structure and Proteomics in Obese Mice

Yang,

Pan,

Chen

2024

DMSO

Self Cite

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This study utilized proteomics to investigate changes in protein expression associated with lung health in obese mice exposed to semaglutide and empagliflozin through a high-fat diet. Methods: Twenty-eight male C57BL/6JC mice were randomly assigned to two groups: a control diet group (n = 7) and a high-fat diet group (n = 21). The HFD group was further divided into three groups: HFD group (n = 7), Sema group (n = 7), and Empa group (n = 7). Post-treatment, mice underwent assessments including glucose tolerance, lipids, oxidative stress markers, body weight, lung weight, and structure. Proteomics identified differentially expressed proteins (DEPs) in lung tissue, and bioinformatics analyzed the biological processes and functions of these proteins. Results: Semaglutide and empagliflozin significantly attenuated obesity-induced hyperglycemia, abnormal lipid metabolism, oxidative stress response, and can decrease alveolar wall thickness, enlarge alveolar lumen, and reduce collagen content in lung tissue. Both medications also attenuated lung elastic fibre cracking and disintegration. In the HFD/NCD group, there were 66 DEPs, comprising 30 proteins that were increased and 36 that were decreased. Twenty-three DEPs overlapped between Sema/HFD and Empa/HFD, with 11 up-regulated and 12 down-regulated simultaneously. After analysing DEPs in different groups, four proteins -LYVE1, BRAF, RGCC, and CHMP5 -were all downregulated in the HFD group and upregulated by semaglutide and empagliflozin treatment. Conclusion:This study demonstrates that obesity induced by a high-fat diet causes a reduction in the expression of LYVE1, BRAF, RGCC, and CHMP5 proteins, potentially affecting lung function and structure in mice. Significantly, the administration of semaglutide and empagliflozin elevates the levels of these proteins, potentially offering therapeutic benefits against lung injury caused by obesity. Merging semaglutide with empagliflozin may exert a more pronounced impact.

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“…By promoting cellular senescence via p16/cyclin D1 pathway, pinX1 suppresses bladder urothelial carcinoma cell proliferation [13]. In recent years, researchers have provided some clues that pinX1 still plays an important role in processes such as inflammatory-related lipopolysaccharide-induced lung injury [14] and lipid metabolism such as obesity-induced cardiac injury [15], nonalcoholic fatty liver disease [16]. PinX1 gene single nucleotide polymorphisms (SNPs) are correlated with serum lipid levels [17].…”

Section: Introductionmentioning

confidence: 99%

PinX1 Alleviates Atherosclerosis by Inhibiting MMP-9 Expression and p66shc-Mediated Oxidative Stress

Yang¹,

Zhang²,

Hong-xia³

et al. 2023

Preprint

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Atherosclerosis (AS) is an age-related disease. Mitochondria and telomere links have been considered to play important roles in AS. PinX1 is a potent and highly conserved endogenous telomerase inhibitor. However, the role of pinX1 in AS and its role in oxidative stress have not been reported. In order to investigate the role of pinX1 in AS, we established a classical AS mice model in the present work and increased pinX1 protein expression using pinX1 overexpression adeno-virus by tail vein injection. Then, red-oil O and HE staining were employed to evaluate the severity of AS. Serum lipid profile and oxidative stress were also detected by using its specific chemical testing kit. The results indicated that high-fat diet (HFD) markedly decreased pinX1 and increased p66shc protein expression, whereas overexpression of pinX1 protein expression in mice produced the opposite results. In addition, pinX1 significantly minimized plaque area and alleviated the abnormal serum lipid profile. By using Western blot and Biochemical assay kits, overexpression of pinX1 decreased p66shc and MMP-9 protein expression and reduced oxidative stress. This study showed pinX1 can inhibit p66shc, MMP-9, and related oxidative stress, pinX1 may be considered as a new candidate target for the treatment of AS.

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UTP14A, DKC1, DDX10, PinX1, and ESF1 Modulate Cardiac Angiogenesis Leading to Obesity-Induced Cardiac Injury

Cited by 10 publications

References 40 publications

Identification of novel prognostic targets in coronary artery disease and related complications using bioinformatics and next generation sequencing data analysis

Identification of novel prognostic targets in coronary artery disease and related complications using bioinformatics and next generation sequencing data analysis

Effect of Semaglutide and Empagliflozin on Pulmonary Structure and Proteomics in Obese Mice

PinX1 Alleviates Atherosclerosis by Inhibiting MMP-9 Expression and p66shc-Mediated Oxidative Stress

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