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May 13, 2026Journal of Cardiothoracic Surgery0 citationsOpen Access

Identification and validation of MYC as an autophagy-related gene for diagnosis and immune infiltration in sepsis-induced myocardial dysfunction

HWHongxia WuKZKe ZhangJWJiangshan Wen

Key Result

MYC was identified as a key autophagy-related gene highly expressed in sepsis-induced myocardial dysfunction, demonstrating excellent diagnostic capability with an AUC of 0.923 in the training dataset.

Key Points

  • This study aims to identify autophagy-related genes for diagnosis in sepsis-induced myocardial dysfunction and explore their immune associations.
  • Conducted bioinformatics analysis using transcriptome data from the GEO database.
  • Identified target autophagy-related genes through weighted gene co-expression network analysis and differential expression analysis.
  • Validated findings using a lipopolysaccharide-induced cell SIMD model.
  • Identified 12 autophagy-related genes associated with SIMD pathogenesis.
  • MYC was the key gene, showing high expression levels and excellent diagnostic capabilities for SIMD.
  • Found significant correlations between MYC expression and immune cell infiltration in SIMD patients.

Structured PICO

P
Population
Human sepsis-induced myocardial dysfunction (SIMD) transcriptome data from the Gene Expression Omnibus (GEO) database and a lipopolysaccharide (LPS)-induced cell SIMD model
I
Intervention
Myc knockdown (in cellular model) and bioinformatics analysis
O
Outcome
Identification of key autophagy-related genes (ARGs) and their diagnostic value in SIMDsurrogate

MYC is identified as a key autophagy-related gene and potential diagnostic marker for sepsis-induced myocardial dysfunction.

Main Result

Effect estimate: AUC 0.923

Abstract

Sepsis-induced myocardial dysfunction (SIMD) is a frequent consequence in septic patients and is correlated with higher mortality. Recent research suggests that activating autophagy might alleviate SIMD. Thus, this study aims to identify the autophagy-related gene (ARG) and assess its diagnostic value in SIMD patients. We conducted a sequential and extensive bioinformatics analysis of human SIMD transcriptome data from the Gene Expression Omnibus (GEO) database. Target ARG in SIMD were identified through weighted gene co-expression network analysis (WGCNA), differential expression analysis, and protein–protein interaction (PPI) network construction. The diagnostic value of the key ARG and its association with immune cell infiltration were evaluated. The role of target ARG in SIMD was validated using a lipopolysaccharide (LPS)-induced cell SMID model. We identified 12 ARGs associated with SIMD pathogenesis based on the human SIMD transcriptome data and investigated their potential biological processes. MYC was identified as a key ARG in SIMD by constructing a protein-protein interaction network. MYC was highly expressed in patients with SIMD and had excellent diagnostic capability for SIMD. Subsequently, we predicted drugs associated with MYC expression and constructed a crucial transcription factor (TF)-miRNA-mRNA co-regulatory network. Finally, we found that several immune-related signaling pathways were significantly activated in the MYChigh group, and MYC was correlated with the infiltration of immune cells in SIMD patients. In an LPS-induced SIMD cellular model, Myc knockdown attenuated the LPS-induced enhancement of autophagic flux. We identified MYC, an autophagy-related gene, as a potential diagnostic marker for SIMD, offering insights into autophagic mechanisms and informing future diagnostic approaches.

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Cite This Study

Wu et al. (2026) studied Sepsis-induced myocardial dysfunction (n=31). MYC expression vs. Healthy controls was evaluated on Diagnostic capability for SIMD (Area Under the Curve) (AUC 0.923). MYC was identified as a key autophagy-related gene highly expressed in sepsis-induced myocardial dysfunction, demonstrating excellent diagnostic capability with an AUC of 0.923 in the training dataset.

synapsesocial.com/papers/6a04153d79e20c90b4444fc6https://doi.org/10.1186/s13019-026-04242-2
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