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Identification and Validation of Ferroptosis-Related Biomarkers in Septic Cardiomyopathy via Bioinformatics Analysis
Cheng-Wu Gong1,2, Ming-Ming Yuan2,3, Bai-Quan Qiu1,2
1Department of Cardiothoracic Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, China.
Insights
This study reveals ferroptosis-related genes (FRGs) play a crucial role in septic cardiomyopathy (SCM), a heart dysfunction linked to sepsis. Identifying these genes offers new insights into SCM
Area of Science:
- Cardiology
- Molecular Biology
- Genetics
Background:
- Septic cardiomyopathy (SCM) is a severe cardiac dysfunction complicating sepsis and septic shock, with unclear molecular mechanisms.
- Ferroptosis, a distinct form of programmed cell death, has been observed in sepsis-related myocardial injury, suggesting its involvement in SCM.
- Understanding the genetic underpinnings of SCM is critical for developing effective treatments.
Purpose of the Study:
- To investigate the role of ferroptosis-related genes (FRGs) in the pathogenesis of septic cardiomyopathy (SCM).
- To identify key ferroptosis-related targets and potential therapeutic strategies for SCM.
- To elucidate the molecular mechanisms underlying SCM by analyzing gene expression and regulatory networks.
Main Methods:
- Bioinformatics analysis to identify differentially expressed genes (DEGs) and ferroptosis-related genes (FRGs) in SCM.
- Identification of hub genes within the FRG dataset and construction of a microRNA-FRG regulatory network.
- Prediction of candidate drugs targeting identified hub genes and validation using qRT-PCR and western blotting.
Main Results:
- Several ferroptosis-related genes (FRGs) were identified as potentially involved in the development of septic cardiomyopathy (SCM).
- Key hub genes and a regulatory network involving microRNAs were pinpointed, suggesting specific molecular pathways.
- Expression levels of identified hub genes were confirmed to be abnormal in the context of SCM.
Conclusions:
- Ferroptosis is implicated as a significant mechanism contributing to myocardial injury in septic cardiomyopathy (SCM).
- The identified FRGs and regulatory networks provide novel molecular targets for understanding and treating SCM.
- This research offers potential therapeutic avenues for mitigating cardiac dysfunction associated with sepsis.
Abstract:
Septic cardiomyopathy (SCM) is a cardiac dysfunction caused by severe sepsis and septic shock that increases the risk of heart failure and death and its molecular mechanism remains unclear. Ferroptosis, a novel form of programmed cell death, has been reported to be present in the heart tissue of patients with sepsis, which demonstrated that ferroptosis may be a potential mechanism of myocardial injury in SCM. Therefore, we explored the role of ferroptosis-related genes (FRGs) in SCM and aimed to identify pivotal ferroptosis-related targets in SCM and potential therapeutic targets involved in the pathological process of SCM. To explore the regulatory mechanisms of ferroptosis in SCM, we identified differentially expressed genes (DEGs) in SCM and FRGs by bioinformatics analysis, and further identified hub genes. And the crucial microRNAs (miRNAs)-FRGs regulatory network was subsequently constructed. Finally, several candidate drugs associated with the hub genes were predicted, and Real-time quantitative reverse Transcription PCR (qRT-PCR) and western blotting analysis were performed to confirm the abnormal expression of hub genes. In this study, we identified several FRGs that may be involved in the pathogenesis of SCM, which helps us further clarify the role of ferroptosis in SCM and deeply understand the molecular mechanisms and potential therapeutic targets of SCM.
