Gradual DNA methylation changes reveal transcription factors implicated in metabolic dysfunction-associated steatotic liver disease progression and epigenetic age acceleration.

Evelien Van Dijck, Steven Van Laere, Emilie Logie, Steven Timmermans, Erik Fransen, Joe Ibrahim, Timothy J Kendall, Jonathan A Fallowfield, Ligia M Mateiu, Claude Libert, Guy Van Camp, An Verrijken, Luc Van Gaal, Sven Francque, Wim Van Hul, Wim Vanden Berghe

Cell Death Signaling-Epigenetics Lab, Department Biomedical Sciences, University of Antwerp, 2610, Wilrijk, Belgium. [email protected] Death Signaling-Epigenetics Lab, Department Biomedical Sciences, University of Antwerp, 2610, Wilrijk, Belgium. [email protected]. · pubmed

Paper

Abstract

Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most common chronic liver disease worldwide, but its pathophysiological mechanisms remain elusive. It is a progressive disease, encompassing hepatic steatosis, steatohepatitis with (out) fibrosis, and ultimately cirrhosis and hepatocellular carcinoma. DNA methylation (DNAm) is dysregulated in MASLD and may play a central role in its pathogenesis. Additionally, aging is associated with MASLD and shares common processes of chronic inflammation and oxidative stress. Therefore, this study focuses on DNAm changes in relation to MASLD progression and epigenetic age acceleration (EAA).

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Research summary

The paper claims that DNA methylation changes are linked to the progression of metabolic dysfunction-associated steatotic liver disease and epigenetic age acceleration. This research is relevant as it explores the epigenetic mechanisms underlying aging-related diseases, potentially addressing root causes of aging through understanding metabolic dysfunction.

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