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Identification of genes and key pathways underlying the pathophysiological association between sarcopenia and chronic

Weixi Wang1, Weiying Ren1, Lin Zhu1

  • 1Department of Geriatrics, Zhongshan Hospital, Fudan University, Shanghai, China.

Experimental Gerontology
|February 6, 2024
PubMed
Summary
This summary is machine-generated.

This study identifies common molecular mechanisms linking chronic obstructive pulmonary disease (COPD) and sarcopenia. Key findings suggest the SAA1 gene and NF-κB pathway are involved, with oxidative phosphorylation and ferroptosis playing significant roles.

Keywords:
Bioinformatics analysisChronic obstructive pulmonary disease (COPD)Hub geneSarcopeniaTranscription factor

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Area of Science:

  • Pulmonary Medicine
  • Geriatrics
  • Molecular Biology

Background:

  • Chronic obstructive pulmonary disease (COPD) is frequently associated with sarcopenia, a condition characterized by muscle loss.
  • The precise molecular mechanisms connecting COPD and sarcopenia remain unclear, necessitating further investigation into shared pathogenetic pathways.

Purpose of the Study:

  • To explore the common genes, signaling pathways, and transcription factors involved in the molecular pathogenesis of sarcopenia and COPD.
  • To identify potential therapeutic targets for managing sarcopenia in COPD patients.

Main Methods:

  • Utilized Gene Expression Omnibus (GEO) datasets (GSE8479 for sarcopenia, GSE76925 for COPD) to identify overlapping differentially expressed genes (DEGs).
  • Conducted comprehensive bioinformatics analyses, including functional annotation, enrichment analyses (GO, KEGG), protein-protein interaction (PPI) network construction, and transcription factor (TF) prediction.
  • Validated key genes and TFs through expression analysis.

Main Results:

  • Identified 118 downregulated and 92 upregulated common DEGs between sarcopenia and COPD.
  • Functional analysis implicated oxidoreductase activity and ferroptosis in the pathogenesis.
  • Thirty hub genes were detected, with ATP metabolic process and oxidative phosphorylation being closely related; SAA1, C3, and ACSS2 were upregulated, while ATF4, PPARGC1A, and MCTS1 were downregulated.
  • Six TFs (NFKB1, RELA, IRF7, SP1, MYC, JUN) were identified, with SAA1 coregulated by NFKB1 and RELA.

Conclusions:

  • Uncovered potential shared molecular mechanisms underlying COPD complicated by sarcopenia.
  • The hub gene SAA1 and the NF-κB signaling pathway are likely involved in this comorbidity.
  • Oxidative phosphorylation and ferroptosis emerge as critical contributors to the pathogenesis of sarcopenia in COPD patients.