Identification of key biomarkers and immune infiltration in the thoracic acute aortic dissection by bioinformatics

Jun Luo1, Haoming Shi2, Haoyu Ran2

  • 1Department of Cardiothoracic Surgery, The First Affiliated Hospital of Chongqing Medical University, No. 1 Youyi Road, Yuzhong District, Chongqing, China.

Insights

Researchers identified two key genes, SLC11A1 and FGL2, involved in thoracic acute aortic dissection (TAAD). These genes may play a role in the immune-inflammatory responses contributing to this fatal cardiovascular disease.

Area of Science:

  • Cardiovascular Research
  • Genomics
  • Immunology

Background:

  • Thoracic acute aortic dissection (TAAD) is a highly fatal cardiovascular disease with unclear underlying mechanisms.
  • Understanding the genetic and molecular basis of TAAD is crucial for identifying potential diagnostic markers and therapeutic targets.

Purpose of the Study:

  • To identify differentially expressed genes (DEGs) associated with TAAD.
  • To screen and validate reliable diagnostic markers for TAAD.
  • To investigate the role of identified genes in immune-inflammatory responses within TAAD tissues.

Main Methods:

  • Utilized three Gene Expression Omnibus datasets to identify DEGs.
  • Employed weighted gene co-expression network analysis to identify functional and co-expression networks.
  • Applied machine learning algorithms (LASSO, Random Forest, SVM-RFE) for marker screening.
  • Validated candidate markers using quantitative real-time PCR (qRT-PCR) and an independent dataset.
  • Analyzed immune cell infiltration in TAAD tissues using CIBERSORT.

Main Results:

  • Identified 25 DEGs, subsequently narrowed down to three candidate genes.
  • Validated SLC11A1 and FGL2 as significantly expressed genes in TAAD through qRT-PCR and an independent dataset.
  • Functional analysis indicated that SLC11A1 and FGL2 are significantly involved in immune-inflammatory responses.

Conclusions:

  • SLC11A1 and FGL2 are differentially expressed in thoracic acute aortic dissection.
  • These genes are potentially implicated in the immune-inflammatory pathways contributing to TAAD pathogenesis.
  • Further research into SLC11A1 and FGL2 could lead to novel diagnostic or therapeutic strategies for TAAD.
Abstract

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