ReviewFrontiers in endocrinology2025
DNA methylation and demethylation in adipocyte biology: roles of DNMT and TET proteins in metabolic disorders.
Review in Frontiers in endocrinology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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.
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.
Who cites it
3 citing papers in PubMed.
- Adipocyte-Derived KIF13B Aggravates Obesity-Associated Metabolic Dysfunction via LRP1/PPARγ Signaling.MedComm · 2026Article
- Article
- Mechanisms and therapeutic prospects of DNA methylation-mucosal innate immunity crosstalk in inflammatory bowel disease.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Adipocytes play a crucial role in regulating energy metabolism throughout the body. Dysfunctional adipocyte biology is a primary factor in the development of metabolic disorders associated with obesity and type 2 diabetes. Over the past decades, the role of epigenetic mechanisms, particularly DNA methylation, in the development and regulation of adipocytes has been extensively elucidated. These mechanisms influence numerous biological processes in adipose tissue and adipocytes, including lipogenesis and lipid metabolism. With the discovery of the active DNA demethylation mechanism centered on ten-eleven translocation (TET) proteins, a growing body of evidence sug-gests that DNA demethylation mechanisms also profoundly influence various aspects of adipocyte biology and regulate cellular differentiation and function by altering the methylation status of genes. Following the discovery of active DNA demethylation mechanisms mediated by TET proteins, a growing body of evidence indicates that these mechanisms profoundly influence multiple aspects of adipocyte biology. Specifically, these mechanisms regulate cellular differentiation and function by altering the methylation status of key genes involved in adipogenesis and metabolism. A precise and detailed understanding of the mechanisms underlying DNA demethylation in adipocyte biology is imperative for the identification of novel interventional therapies targeting adipocyte gene methylation and demethylation. This review examines the specific molecular mechanisms and significance of passive and active DNA demethylation in adipocyte biology, focusing on the DNA methyltransferase family and TET proteins. It summarizes crosstalk mechanisms involving DNA methyltransferases, highlights the multiple action pathways of TET proteins, and reveals the potential of additional intervention pathways. This review aims to provide an updated theoretical basis for promising therapeutic targets.
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Registered trials
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