Evidence map›Paper›PMID 41664704›Full record

ReviewFrontiers in genetics2026

The mechanism and clinical significance of FKBP5 gene DNA methylation in various psychiatric, metabolic and tumor-related diseases.

Changliang Wang, Zhixiu Xia

Abstract readReview
In one paragraph

Review in Frontiers in genetics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Changliang WangJudicial Authentication Center, The People's Procuratorate of Liaoning Province, Collaborative Laboratory of Intelligentized Forensic Science (CLIFS), Shenyang, China.
Zhixiu Xia *Department of General Surgery, Shengjing Hospital of China Medical University, Shenyang, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The FK506 Binding Protein 5 (FKBP5) gene encodes a protein that binds to the immunosuppressive agent FK506. FKBP5 expression is regulated by genetic variation and epigenetic mechanisms, including DNA methylation (DNAm). This gene regulates the glucocorticoid receptor (GR), and aberrant FKBP5 methylation is associated with psychiatric and metabolic disorders. Recent evidence also indicates that FKBP5 methylation significantly influences malignant tumors. The methylation status of FKBP5 not only modulates its own expression but also contributes to disease pathogenesis by regulating downstream signaling pathways. Despite extensive research on FKBP5 in individual disease contexts, a critical gap remains in understanding how its DNAm serves as a unifying epigenetic mechanism across psychiatric, metabolic, and neoplastic disorders. Existing reviews often focus on single disease domains or on genetic and protein-level regulation, lacking a systematic, horizontal integration analysis centered on DNAm-a dynamic and reversible modification. This review aims to fill this gap by proposing a coherent "epigenetic regulatory framework" that elucidates how tissue-and site-specific FKBP5 DNAm patterns, through modulating glucocorticoid (GC) signaling, stress responses, and inflammatory pathways (e.g., NF-κB), contribute to divergent pathological outcomes. By integrating evidence from disparate fields, this review summarizes the role of FKBP5 DNAm in disease biology, its functions across various disorders, and its potential as a biomarker and therapeutic target, aiming to provide a theoretical foundation and strategic insights for disease diagnosis and treatment.

Indexed as

biomarkerDNA methylationepigeneticsFKBP5targeted therapy

Identifiers

PMID41664704
PMCPMC12883251

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.