ArticleEuropean journal of endocrinology2022
Identification of glucocorticoid-related molecular signature by whole blood methylome analysis.
Article in European journal of endocrinology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 14 citations in OpenAlex.
- Cognitive Assessment in Adults With Adrenal Cortisol Insufficiency: Challenges and Opportunities.Endocrine reviews · 2026Review
- Development and evaluation of a machine learning based risk prediction model for osteoporosis.Frontiers in molecular biosciences · 2026Article
- The mechanism and clinical significance of FKBP5 gene DNA methylation in various psychiatric, metabolic and tumor-related diseases.Frontiers in genetics · 2026Review
- Impact of steroid differentiation on tumor microenvironment revealed by single-nucleus atlas of adrenal tumors.Nature communications · 2025Article
- Steroid hormone-mediated epigenetic programming during puberty: uncovering links to depression.Epigenomics · 2025Review
- Epigenetic Mechanisms Modulated by Glucocorticoids With a Focus on Cushing Syndrome.The Journal of clinical endocrinology and metabolism · 2024Review
- Blood DNA methylation ofFrontiers in epigenetics and epigenomics · 2024Article
- Biomarkers of aging through the life course: A Recent Literature Update.Current opinion in epidemiology and public health · 2023Article
- Pitfalls in the Diagnosis and Management of Hypercortisolism (Cushing Syndrome) in Humans; A Review of the Laboratory Medicine Perspective.Diagnostics (Basel, Switzerland) · 2023Review
- In Situ Metabolomics of Cortisol-Producing Adenomas.Clinical chemistry · 2023Article
- Whole blood methylome-derived features to discriminate endocrine hypertension.Clinical epigenetics · 2022Article
- Evaluation of cross-platform compatibility of a DNA methylation-based glucocorticoid response biomarker.Clinical epigenetics · 2022Article
Corrections and comments
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Authors and funding
24 authors at 6 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveCushing's syndrome represents a state of excessive glucocorticoids related to glucocorticoid treatments or to endogenous hypercortisolism. Cushing's syndrome is associated with high morbidity, with significant inter-individual variability. Likewise, adrenal insufficiency is a life-threatening condition of cortisol deprivation. Currently, hormone assays contribute to identify Cushing's syndrome or adrenal insufficiency. However, no biomarker directly quantifies the biological glucocorticoid action. The aim of this study was to identify such markers.
designWe evaluated whole blood DNA methylome in 94 samples obtained from patients with different glucocorticoid states (Cushing's syndrome, eucortisolism, adrenal insufficiency). We used an independent cohort of 91 samples for validation.
methodsLeukocyte DNA was obtained from whole blood samples. Methylome was determined using the Illumina methylation chip array (~850 000 CpG sites). Both unsupervised (principal component analysis) and supervised (Limma) methods were used to explore methylome profiles. A Lasso-penalized regression was used to select optimal discriminating features.
resultsWhole blood methylation profile was able to discriminate samples by their glucocorticoid status: glucocorticoid excess was associated with DNA hypomethylation, recovering within months after Cushing's syndrome correction. In Cushing's syndrome, an enrichment in hypomethylated CpG sites was observed in the region of FKBP5 gene locus. A methylation predictor of glucocorticoid excess was built on a training cohort and validated on two independent cohorts. Potential CpG sites associated with the risk for specific complications, such as glucocorticoid-related hypertension or osteoporosis, were identified, needing now to be confirmed on independent cohorts.
conclusionsWhole blood DNA methylome is dynamically impacted by glucocorticoids. This biomarker could contribute to better assessment of glucocorticoid action beyond hormone assays.
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