Integrative bioinformatics analysis reveals STAT2 as a novel biomarker of inflammation-related cardiac dysfunction in

Cairong Li1, Guanhua Li1, Sijia Tu1

  • 1Department of Cardiology, First People's Hospital of Linping District, Hangzhou 311199, P.R. China.

PubMed

Insights

Atrial fibrillation (AF) and COVID-19 share common risk genes, including STAT2. Silencing STAT2 improved cardiac function in vitro, suggesting STAT2 as a potential biomarker for inflammation-related cardiac dysfunction in AF.

Area of Science:

  • Cardiology
  • Virology
  • Genomics

Background:

  • Atrial fibrillation (AF) is a major cause of stroke and cardiac dysfunction.
  • Viral infections, particularly COVID-19, can exacerbate AF and increase mortality through inflammation.
  • Understanding the molecular links between viral infections and AF is crucial.

Purpose of the Study:

  • To identify shared genetic risk factors between AF and COVID-19.
  • To investigate the role of these genes in cardiac dysfunction.
  • To explore potential therapeutic targets for AF in the context of viral infections.

Main Methods:

  • Utilized weighted gene co-expression network analysis on AF and COVID-19 databases.
  • Identified common risk genes in heart tissues and peripheral blood mononuclear cells.
  • Performed in vitro experiments involving STAT2 silencing and viral pseudovirus exposure.

Main Results:

  • Identified HSCT, PSMB9, STAT2, and TNFSF13B as common risk genes for AF and COVID-19.
  • Demonstrated a positive correlation between these genes and disease relevance.
  • Showed that STAT2 silencing rescued cardiac cell contraction dysfunction induced by SARS-CoV-2 XBB1.5 pseudovirus.

Conclusions:

  • STAT2 is a potential novel biomarker for inflammation-related cardiac dysfunction in AF patients.
  • Shared genetic pathways may link viral infections like COVID-19 to AF pathogenesis.
  • Targeting STAT2 could offer a therapeutic strategy for AF with viral triggers.

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