SGK1 linked to myeloid cell senescence markers in ME/CFS: transcriptomic and cell-model study
In an abstract of an integrative transcriptomic and cell-model study, SGK1 was identified as a candidate regulator associated with myeloid cell senescence-related alterations in ME/CFS; the authors call for validation in primary patient immune cells and clinical cohorts. [1]
Automatic summary · not editorially reviewed
The key findings
The authors used bulk transcriptomic dataset GSE14577 and intersected ME/CFS-correlated gene modules with aging-related genes from the GenAge database to obtain candidate genes. [1]
Single-cell RNA sequencing data suggested SGK1 expression was enriched in myeloid cell populations, including monocytes and neutrophils, in individuals with ME/CFS. [1]
In D-galactose-induced senescent THP-1 cells, SGK1 knockdown markedly reduced mRNA levels of the senescence markers p16, p21 and p53. [1]
The source at a glance
- Study type / format
- Integrative transcriptomic and computational study with in vitro cell-model validation (abstract)
- Population / context
- People with ME/CFS in public transcriptomic datasets and D-galactose-induced senescent THP-1 cells in vitro
- Summary based on
- Study abstract
- Original publication
- October 16, 2026
ME/CFS transcriptomes screened for aging-related hub genes
The authors describe ME/CFS as a complex illness without objective diagnostic biomarkers or a clear understanding of its pathophysiology, with immune dysregulation and chronic inflammation resembling aging phenotypes. They asked whether myeloid cell senescence plays a role, which they say had not been explored. Using the bulk transcriptomic dataset GSE14577, they identified differentially expressed genes and used weighted gene co-expression network analysis to find modules correlated with the ME/CFS phenotype. Candidate genes came from intersecting these modules with aging-related genes from the GenAge database.
Supporting source [1]
SGK1 enriched in myeloid cells; knockdown lowered p16, p21, p53
Core hub genes were selected using LASSO regression and random forest machine learning; HMGCR and SGK1 emerged. Functional enrichment linked candidate genes to cellular senescence and inflammation pathways. Single-cell RNA sequencing data (GSE214283) suggested SGK1 expression was enriched in myeloid cell populations, including monocytes and neutrophils, in individuals with ME/CFS, whereas HMGCR showed a broader pattern. Single-gene analysis associated SGK1 with autophagy and lysosomal function. In vitro, SGK1 was significantly upregulated in D-galactose-induced senescent THP-1 cells, and SGK1 knockdown markedly reduced mRNA levels of the senescence markers p16, p21 and p53.
Supporting source [1]
Candidate link only; primary patient cells and cohorts untested
The authors conclude that SGK1 is a candidate molecule associated with myeloid cell senescence-related alterations in ME/CFS, and that the integrated analyses suggest a potential link between SGK1 expression and aging-associated immune alterations. They state that further validation in primary ME/CFS-derived immune cells and clinical cohorts is required to determine the biological significance and clinical relevance of SGK1. This is an abstract; the full text was not reviewed. The described work is an association and cell-model study, not evidence that SGK1 causes ME/CFS or that modifying it benefits patients.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. Findings come from bioinformatic analyses of public datasets and an in vitro THP-1 cell senescence model. The authors state that validation in primary ME/CFS-derived immune cells and clinical cohorts is required. Associations do not establish causation or clinical benefit.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Jin Y, Qin R, Li W, Liu J, Chen X. · europepmc.org · October 16, 2026