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

BACKGROUND: This study is aimed at exploring the key genes and the possible mechanism of heart damage caused by obesity. METHODS: We analyzed the GSE98226 dataset. Firstly, differentially expressed genes (DEGs) were identified in heart tissues of obese and normal mice. Then, we analyzed DEGs using G...

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Autores principales: Pan, Xiaoyu, Chen, Shuchun, Chen, Xing, Ren, Qingjuan, Yue, Lin, Niu, Shu, Li, Zelin, Zhu, Ruiyi, Chen, Xiaoyi, Jia, Zhuoya, Zhen, Ruoxi, Ban, Jiangli
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9208995/
https://www.ncbi.nlm.nih.gov/pubmed/35734237
http://dx.doi.org/10.1155/2022/2923291
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author Pan, Xiaoyu
Chen, Shuchun
Chen, Xing
Ren, Qingjuan
Yue, Lin
Niu, Shu
Li, Zelin
Zhu, Ruiyi
Chen, Xiaoyi
Jia, Zhuoya
Zhen, Ruoxi
Ban, Jiangli
author_facet Pan, Xiaoyu
Chen, Shuchun
Chen, Xing
Ren, Qingjuan
Yue, Lin
Niu, Shu
Li, Zelin
Zhu, Ruiyi
Chen, Xiaoyi
Jia, Zhuoya
Zhen, Ruoxi
Ban, Jiangli
author_sort Pan, Xiaoyu
collection PubMed
description BACKGROUND: This study is aimed at exploring the key genes and the possible mechanism of heart damage caused by obesity. METHODS: We analyzed the GSE98226 dataset. Firstly, differentially expressed genes (DEGs) were identified in heart tissues of obese and normal mice. Then, we analyzed DEGs using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis. Thirdly, we constructed a protein-protein interaction (PPI) network and key modules and searched hub genes. Finally, we observed the pathological changes associated with obesity through histopathology. RESULTS: A total of 763 DEGs were discovered, including 629 upregulated and 134 downregulated genes. GO enrichment analysis showed that these DEGs were mainly related to the regulation of transcription, DNA-templated, nucleic acid binding, and metal ion binding. KEGG pathway analysis revealed that the DEGs were enriched in long-term depression, gap junction, and sphingolipid signaling pathways. Finally, we identified UTP14A, DKC1, DDX10, PinX1, and ESF1 as the hub genes. Histopathologic analysis showed that obesity increased the number of collagen fibers and decreased the number of microvessels and proliferation of the endothelium and increased endothelial cell damage which further leads to dysfunction of cardiac microcirculation. CONCLUSION: UTP14A, DKC1, DDX10, PinX1, and ESF1 have been identified as hub genes in obesity-induced pathological changes in the heart and may be involved in obesity-induced cardiac injury by affecting cardiac microcirculatory function.
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spelling pubmed-92089952022-06-21 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 J Diabetes Res Research Article BACKGROUND: This study is aimed at exploring the key genes and the possible mechanism of heart damage caused by obesity. METHODS: We analyzed the GSE98226 dataset. Firstly, differentially expressed genes (DEGs) were identified in heart tissues of obese and normal mice. Then, we analyzed DEGs using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis. Thirdly, we constructed a protein-protein interaction (PPI) network and key modules and searched hub genes. Finally, we observed the pathological changes associated with obesity through histopathology. RESULTS: A total of 763 DEGs were discovered, including 629 upregulated and 134 downregulated genes. GO enrichment analysis showed that these DEGs were mainly related to the regulation of transcription, DNA-templated, nucleic acid binding, and metal ion binding. KEGG pathway analysis revealed that the DEGs were enriched in long-term depression, gap junction, and sphingolipid signaling pathways. Finally, we identified UTP14A, DKC1, DDX10, PinX1, and ESF1 as the hub genes. Histopathologic analysis showed that obesity increased the number of collagen fibers and decreased the number of microvessels and proliferation of the endothelium and increased endothelial cell damage which further leads to dysfunction of cardiac microcirculation. CONCLUSION: UTP14A, DKC1, DDX10, PinX1, and ESF1 have been identified as hub genes in obesity-induced pathological changes in the heart and may be involved in obesity-induced cardiac injury by affecting cardiac microcirculatory function. Hindawi 2022-06-13 /pmc/articles/PMC9208995/ /pubmed/35734237 http://dx.doi.org/10.1155/2022/2923291 Text en Copyright © 2022 Xiaoyu Pan et al. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Pan, Xiaoyu
Chen, Shuchun
Chen, Xing
Ren, Qingjuan
Yue, Lin
Niu, Shu
Li, Zelin
Zhu, Ruiyi
Chen, Xiaoyi
Jia, Zhuoya
Zhen, Ruoxi
Ban, Jiangli
UTP14A, DKC1, DDX10, PinX1, and ESF1 Modulate Cardiac Angiogenesis Leading to Obesity-Induced Cardiac Injury
title UTP14A, DKC1, DDX10, PinX1, and ESF1 Modulate Cardiac Angiogenesis Leading to Obesity-Induced Cardiac Injury
title_full UTP14A, DKC1, DDX10, PinX1, and ESF1 Modulate Cardiac Angiogenesis Leading to Obesity-Induced Cardiac Injury
title_fullStr UTP14A, DKC1, DDX10, PinX1, and ESF1 Modulate Cardiac Angiogenesis Leading to Obesity-Induced Cardiac Injury
title_full_unstemmed UTP14A, DKC1, DDX10, PinX1, and ESF1 Modulate Cardiac Angiogenesis Leading to Obesity-Induced Cardiac Injury
title_short UTP14A, DKC1, DDX10, PinX1, and ESF1 Modulate Cardiac Angiogenesis Leading to Obesity-Induced Cardiac Injury
title_sort utp14a, dkc1, ddx10, pinx1, and esf1 modulate cardiac angiogenesis leading to obesity-induced cardiac injury
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9208995/
https://www.ncbi.nlm.nih.gov/pubmed/35734237
http://dx.doi.org/10.1155/2022/2923291
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