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pmid:35957694

Identification of novel biomarkers in septic cardiomyopathy via integrated bioinformatics analysis and experimental validation.

Feng Lu · Feng Hu · Baiquan Qiu · Hongpeng Zou · Jianjun Xu

Frontiers in genetics · 2022 doi:10.3389/fgene.2022.929293

Paper

complete

Experiment

partial

Data

partial

Analysis

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Identification of novel biomarkers in septic cardiomyopathy via integrated bioinformatics analysis and experimental validation.
doi
10.3389/fgene.2022.929293
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Feng Lu
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Feng Hu
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Baiquan Qiu
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Hongpeng Zou
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Jianjun Xu
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Frontiers in genetics
year
2022
abstract
Purpose: Septic cardiomyopathy (SCM) is an important world public health problem with high morbidity and mortality. It is necessary to identify SCM biomarkers at the genetic level to identify new therapeutic targets and strategies. Method: DEGs in SCM were identified by comprehensive bioinformatics analysis of microarray datasets (GSE53007 and GSE79962) downloaded from the GEO database. Subsequently, bioinformatics analysis was used to conduct an in-depth exploration of DEGs, including GO and KEGG pathway enrichment analysis, PPI network construction, and key gene identification. The top ten Hub genes were identified, and then the SCM model was constructed by treating HL-1 cells and AC16 cells with LPS, and these top ten Hub genes were examined using qPCR. Result: STAT3, SOCS3, CCL2, IL1R2, JUNB, S100A9, OSMR, ZFP36, and HAMP were significantly elevated in the established SCM cells model. Conclusion: After bioinformatics analysis and experimental verification, it was demonstrated that STAT3, SOCS3, CCL2, IL1R2, JUNB, S100A9, OSMR, ZFP36, and HAMP might play important roles in SCM.
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After data preprocessing, DEGs were analyzed using the limma package of R software (version 4.2.1).
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Nine hub genes were significantly elevated in the LPS-treated HL-1 and AC16 cell septic cardiomyopathy models: STAT3, SOCS3, CCL2, IL1R2, JUNB, S100A9, OSMR, ZFP36, and HAMP.
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Nine hub genes were significantly elevated in the LPS-treated HL-1 cell SCM model, including STAT3, SOCS3, CCL2, IL1R2, JUNB, S100A9, OSMR, ZFP36, and HAMP (Figure 5A). The same results were obtained in the SCM model constructed by LPS-treated AC16 cells (Figure 5B).
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Complete file
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It is necessary to identify SCM biomarkers at the genetic level to identify new therapeutic targets and strategies. Method: DEGs in SCM were identified by comprehensive bioinformatics analysis of microarray datasets (GSE53007 and GSE79962) downloaded from the GEO database. Subsequently, bioinformatics analysis was used to conduct an in-depth exploration of DEGs, including GO and KEGG pathway enrichment analysis, PPI network construction, and key gene identification. The top ten Hub genes were identified, and then the SCM model was constructed by treating HL-1 cells and AC16 cells with LPS, and these top ten Hub genes were examined using qPCR. Result: STAT3, SOCS3, CCL2, IL1R2, JUNB, S100A9, OSMR, ZFP36, and HAMP were significantly elevated in the established SCM cells model. 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