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Exploring Dysregulated Ferroptosis-Related Genes in Septic Myocardial Injury Based on Human Heart Transcriptomes:
Hua-Xi Zou1,2, Tie Hu1,2, Jia-Yi Zhao2,3
1Department of Cardiovascular Surgery, The First Affiliated Hospital of Nanchang University, Nanchang, People's Republic of China.
Journal of Inflammation Research
|March 16, 2023
Summary
Ferroptosis, a cell death pathway, is implicated in septic myocardial injury (SMI). This study identifies key ferroptosis genes in human hearts, offering new diagnostic and therapeutic targets for sepsis.
Area of Science:
- Cardiovascular Biology
- Cell Death Mechanisms
- Bioinformatics
Background:
- Sepsis frequently causes cardiac dysfunction (septic myocardial injury, SMI), impacting patient prognosis.
- Ferroptosis, a form of programmed cell death involving iron and lipid peroxidation, is increasingly recognized as a factor in SMI.
- Understanding ferroptosis in human SMI is limited, lacking direct evidence from cardiac tissue.
Purpose of the Study:
- To investigate the role of ferroptosis in human septic myocardial injury.
- To identify key ferroptosis-related genes (FRGs) and their mechanisms in SMI.
- To explore potential diagnostic and therapeutic strategies for SMI based on ferroptosis.
Main Methods:
- Comprehensive bioinformatics analysis of human sepsis cardiac transcriptome data.
- Utilized the lipopolysaccharide-induced mouse SMI model for validation.
- Constructed protein-protein interaction networks to identify key genes and modules.
Main Results:
- Identified widespread dysregulation of ferroptosis-related genes in human SMI.
- Eight key FRGs (HIF1A, MAPK3, NOX4, PPARA, PTEN, RELA, STAT3, TP53) were identified as regulators of ferroptosis in SMI.
- Key FRGs demonstrated diagnostic capabilities for SMI and were linked to patient prognosis and immune infiltration.
Conclusions:
- This study provides human cardiac transcriptome evidence for ferroptosis's role in SMI.
- The findings offer new insights into SMI pathobiology.
- Identified key FRGs and potential ferroptosis-modulating drugs as promising targets for SMI diagnosis and treatment.