Skip to content
DraconiticResearch
Search Sources API
203,234 studies31 sourcesUpdated 16 min ago
Peer-reviewedCC BY 4.0PLOS One

Identification of SGK1 as a candidate regulator associated with myeloid cell senescence in ME/CFS: An integrative transcriptomic and experimental study

  • Yan Jin1
  • Rui Qin2
  • Wan Li
  • Jin Liu
  • Xinghua Chen
  1. 1The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China
  2. 2Guangzhou University of Chinese Medicine, Guangzhou, China
Open at sourcePDFDOICite

Abstract

Background: Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a complex illness lacking objective diagnostic biomarkers and clear pathophysiological understanding. Patients exhibit immune dysregulation and chronic inflammation reminiscent of aging phenotypes, yet the role of myeloid cell senescence in this disease remains unexplored. Methods: A stepwise integrative transcriptomic and computational strategy was employed. Differentially expressed genes were identified from the bulk transcriptomic dataset GSE14577. Weighted gene co-expression network analysis was performed to identify key modules correlated with the ME/CFS phenotype. Candidate genes were obtained by intersecting these modules with aging-related genes from the GenAge database. Core hub genes were further selected using LASSO regression and random forest machine learning algorithms. Cell type-specific expression was mapped using single-cell RNA sequencing data GSE214283, and functional validation was conducted via siRNA knockdown in a THP-1 cell senescence model. Results: Integrative analysis identified HMGCR and SGK1 as core hub genes. Functional enrichment analysis revealed that candidate genes were enriched in pathways related to cellular senescence and inflammation. Single-cell transcriptomics analysis suggested that SGK1 expression was enriched in myeloid cell populations, including monocytes and neutrophils, in individuals with ME/CFS, whereas HMGCR showed a broader expression pattern. Single-gene GSEA indicated that SGK1 was associated with autophagy and lysosomal function. In vitro experiments showed that SGK1 expression was significantly upregulated in D-galactose-induced senescent THP-1 cells, and SGK1 knockdown markedly reduced the mRNA expression levels of senescence markers p16, p21, and p53. Conclusion: This study identifies SGK1 as a candidate molecule associated with myeloid cell senescence-related alterations in ME/CFS. Integrated transcriptomic, single-cell, and experimental analyses suggest a potential link between SGK1 expression and aging-associated immune alterations. However, further validation in primary ME/CFS-derived immune cells and clinical cohorts is required to determine the biological significance and clinical relevance of SGK1.

Related

  1. Identification of Crohn’s disease-associated molecular signatures by integrative bioinformatics analysis and experimental validation
    Peihong Li, Siqing Guo, Hongyi Hu +5
    Frontiers in immunologyPeer-reviewedCC BYFull textImmunologyEurope PMC
  2. Integrative single-cell and bulk transcriptomic analysis identifies monocyte/macrophage senescence-associated candidate genes in pulmonary arterial hypertension
    Xiaojun Chen, Weibin Wu, Yilong Liu +2
    Frontiers in ImmunologyPeer-reviewedCC BY 4.0Full textImmunologyPMCCrossrefEurope PMC
  3. Integrative single-cell and bulk transcriptomic analysis identify R-loop-associated gene signatures driving immune-inflammatory networks in acute pancreatitis
    Lujuan Pan, Weibang Wu, Tianying Zhang +5
    Frontiers in immunologyPeer-reviewedCC BYFull textImmunologyEurope PMC
  4. Identification of Mitochondrial-Lipid Metabolism-Related Diagnostic Targets in Osteoarthritis: Integrative Multi-omics Data and Experimental Validation
    M. Huang, X. Tan, J.-B. Yang +2
    bioRxivPreprintCC BYFull textCell biologybioRxiv
  5. Integrative genomics and experimental validation identify a mechanosensitive gene signature associated with colorectal cancer liver metastasis
    Tianxue Yang, Ye Yuan, Xue Li +3
    iSciencePeer-reviewedCC BY 4.0Full textCell biologyGenetics & genomicsCell PressPMCCrossrefEurope PMC

Cite

BibTeXRIS
BibTeX
@article{jin2026identification,
  title = {{Identification of SGK1 as a candidate regulator associated with myeloid cell senescence in ME/CFS: An integrative transcriptomic and experimental study}},
  author = {Yan Jin and Rui Qin and Wan Li and Jin Liu and Xinghua Chen},
  journal = {PLOS One},
  year = {2026},
  month = oct,
  doi = {10.1371/journal.pone.0359082},
  url = {https://doi.org/10.1371/journal.pone.0359082},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Identification of SGK1 as a candidate regulator associated with myeloid cell senescence in ME/CFS: An integrative transcriptomic and experimental study
AU  - Yan Jin
AU  - Rui Qin
AU  - Wan Li
AU  - Jin Liu
AU  - Xinghua Chen
PY  - 2026
DA  - 2026/10/16
JO  - PLOS One
DO  - 10.1371/journal.pone.0359082
UR  - https://doi.org/10.1371/journal.pone.0359082
AB  - Background: Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a complex illness lacking objective diagnostic biomarkers and clear pathophysiological understanding. Patients exhibit immune dysregulation and chronic inflammation reminiscent of aging phenotypes, yet the role of myeloid cell senescence in this disease remains unexplored. Methods: A stepwise integrative transcriptomic and computational strategy was employed. Differentially expressed genes were identified from the bulk transcriptomic dataset GSE14577. Weighted gene co-expression network analysis was performed to identify key modules correlated with the ME/CFS phenotype. Candidate genes were obtained by intersecting these modules with aging-related genes from the GenAge database. Core hub genes were further selected using LASSO regression and random forest machine learning algorithms. Cell type-specific expression was mapped using single-cell RNA sequencing data GSE214283, and functional validation was conducted via siRNA knockdown in a THP-1 cell senescence model. Results: Integrative analysis identified HMGCR and SGK1 as core hub genes. Functional enrichment analysis revealed that candidate genes were enriched in pathways related to cellular senescence and inflammation. Single-cell transcriptomics analysis suggested that SGK1 expression was enriched in myeloid cell populations, including monocytes and neutrophils, in individuals with ME/CFS, whereas HMGCR showed a broader expression pattern. Single-gene GSEA indicated that SGK1 was associated with autophagy and lysosomal function. In vitro experiments showed that SGK1 expression was significantly upregulated in D-galactose-induced senescent THP-1 cells, and SGK1 knockdown markedly reduced the mRNA expression levels of senescence markers p16, p21, and p53. Conclusion: This study identifies SGK1 as a candidate molecule associated with myeloid cell senescence-related alterations in ME/CFS. Integrated transcriptomic, single-cell, and experimental analyses suggest a potential link between SGK1 expression and aging-associated immune alterations. However, further validation in primary ME/CFS-derived immune cells and clinical cohorts is required to determine the biological significance and clinical relevance of SGK1.
SN  - 1932-6203
ER  -