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Shared genes and relevant potential molecular linkages between COVID-19 and chronic thromboembolic pulmonary

Qianqian Li1, Xia Shi2, Yang Tang3

  • 1Geriatrics Department, Hainan Provincial Hospital of Traditional Chinese Medicine, Haikou , 570203, China.

Journal of Thrombosis and Thrombolysis
|February 1, 2025
PubMed

Insights

This study reveals shared molecular pathways between chronic thromboembolic pulmonary hypertension (CTEPH) and long-COVID, identifying key genes and immune cell regulators. Findings suggest common disease mechanisms and potential therapeutic targets for both conditions.

Area of Science:

  • Genomics
  • Molecular Biology
  • Pulmonary Medicine

Background:

  • Chronic thromboembolic pulmonary hypertension (CTEPH) and COVID-19 (coronavirus disease 2019) share potential molecular links.
  • The interrelation and shared pathogenetic mechanisms between CTEPH and long-COVID remain inadequately understood.

Purpose of the Study:

  • To identify shared molecular pathways and key genes between CTEPH and long-COVID.
  • To explore potential diagnostic and therapeutic strategies by analyzing molecular similarities.

Main Methods:

  • RNA sequencing (RNA-seq) data analysis of CTEPH and long-COVID cohorts (GSE130391, GSE169687).
  • Weighted Gene Co-Expression Network Analysis (WGCNA) to identify key module genes.
  • Differential gene expression analysis, hub gene identification, enrichment analysis, immune cell profiling, and drug prediction.

Main Results:

  • Identified 645 (long-COVID 16 weeks), 206 (long-COVID 24 weeks), and 1,543 differentially expressed genes (DEGs) in CTEPH.
  • Discovered 234 intersecting key module genes and three hub genes (DNAJA1, NDUFA5, SLC2A14) with high discriminatory power (AUC ≥ 0.7).
  • Revealed shared pathways in immune modulation, oxidative stress, and metabolic dysfunction, with activated CD8 T cells as critical regulators. Identified STAT1 and hsa-mir-23a-3p in regulatory networks and predicted potential therapeutics.

Conclusions:

  • Unraveled critical molecular linkages and shared pathogeneses between CTEPH and long-COVID.
  • Highlights the role of immune modulation, oxidative stress, and metabolic dysfunction in both conditions.
  • Provides a foundation for experimental validation and development of novel diagnostic and therapeutic strategies for CTEPH and COVID-19 sequelae.

Keywords:
Bioinformatics analysesCOVID-19Chronic thromboembolic pulmonary hypertensionProtein–protein interaction networkSystems biology

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