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Author Spotlight: Uncovering the Role of Mitochondrial Calcium Phosphate in Heart Failure and Bioenergetics
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The molecular mechanism of cardiac injury in SARS-CoV-2 infection: Focus on mitochondrial dysfunction

Yang Shen1, Min Chen1, Wei Gu2

  • 1Department of Pharmacy, Shanghai University of Medicine & Health Sciences Affiliated Zhoupu Hospital, Shanghai, China.

Journal of Infection and Public Health
|March 23, 2023
PubMed

Insights

Severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) infection triggers mitochondrial dysfunction and NF-κB activation in cardiomyocytes, leading to cardiac injury. This study identifies key molecular mechanisms and potential therapeutic targets for COVID-19-related heart problems.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Virology

Background:

  • Coronavirus disease 2019 (COVID-19) has caused widespread global infections.
  • Cardiac injury is a significant complication affecting patient prognosis and quality of life post-COVID-19.

Purpose of the Study:

  • To elucidate the molecular mechanisms underlying cardiac injury induced by SARS-CoV-2 infection.
  • To identify potential therapeutic strategies for COVID-19-associated cardiac damage.

Main Methods:

  • Utilized RNA-Seq data (GSE184715) comparing SARS-CoV-2 infected and mock human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs).
  • Identified differentially expressed genes (DEGs) and analyzed affected pathways through enrichment analysis.
  • Constructed a protein-protein interaction (PPI) network to identify hub genes and employed Connectivity Map for drug screening.

Main Results:

  • Identified 2705 DEGs, revealing SARS-CoV-2 induced mitochondrial dysfunction, suppressed cardiac muscle contraction, and activated NF-κB.
  • Pinpointed 15 downregulated hub genes primarily involved in mitochondrial respiratory chain complex dysfunction.
  • Discovered 5 candidate drugs for treating COVID-19-induced cardiac injury.

Conclusions:

  • SARS-CoV-2 infection disrupts cardiomyocyte mitochondrial function, reducing respiratory chain activity and ATP synthesis, leading to apoptosis.
  • Activated NF-κB signaling contributes to cytokine storms and exacerbates cardiac injury.
  • The study provides insights into molecular pathways of cardiac damage and suggests potential therapeutic interventions.
Abstract

Keywords:
BioinformaticsCardiac injurySARA-CoV-2

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