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DNA methylation in human lipid metabolism and related diseases.

Curr. Opin. Lipidol. 29, 116-124 (2018)
Verlagsversion DOI
Open Access Gold (Paid Option)
Creative Commons Lizenzvertrag
Purpose of review It is becoming increasingly evident that epigenetic mechanisms, particularly DNA methylation, play a role in the regulation of blood lipid levels and lipid metabolism-linked phenotypes and diseases. Recent findings Recent genome-wide methylation and candidate gene studies of blood lipids have highlighted several robustly replicated methylation markers across different ethnicities. Furthermore, many of these lipid-related CpG sites associated with blood lipids are also linked to lipid-related phenotypes and diseases. Integrating epigenome-wide association studies (EWAS) data with other layers of molecular data such as genetics or the transcriptome, accompanied by relevant statistical methods (e.g. Mendelian randomization), provides evidence for causal relationships. Recent data suggest that epigenetic changes can be consequences rather than causes of dyslipidemia. There is sparse information on many lipid classes and disorders of lipid metabolism, and also on the interplay of DNA methylation with other epigenetic layers such as histone modifications and regulatory RNAs. Summary The current review provides a literature overview of epigenetic modifications in lipid metabolism and other lipid-related phenotypes and diseases focusing on EWAS of DNA methylation from January 2016 to September 2017. Recent studies strongly support the importance of epigenetic modifications, such as DNA methylation, in lipid metabolism and related diseases for relevant biological insights, reliable biomarkers, and even future therapeutics.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Review
Schlagwörter Dna Methylation ; Lipid Metabolism ; Ewas ; Blood Lipids; Epigenome-wide Association; Body-mass Index; Coronary-artery-disease; Mendelian Randomization; Integrative Analysis; Waist Circumference; Cpt1a Locus; Blood; Risk; Obesity
ISSN (print) / ISBN 0957-9672
e-ISSN 1473-6535
Quellenangaben Band: 29, Heft: 2, Seiten: 116-124 Artikelnummer: , Supplement: ,
Verlag Lippincott Williams & Wilkins
Verlagsort Philadelphia
Begutachtungsstatus Peer reviewed