Proceedings of the International scientific and practical conference ―New York Global Science Conference 2026‖ (March 6-8, 2026) / Publisher website: www.naukainfo.com. – New York, USA, 2026. - 250 p.

200 critical mechanistic link in this context. Growing evidence supports the pivotal role of epigenetic mechanisms in the initiation, progression, and clinical heterogeneity of MASLD. Keywords: metabolic dysfunction-associated steatotic liver disease, metabolic dysfunction-associated steatohepatitis, epigenetic, histone methylation, histone acetylation, histone phosphorylation, histone ubiquitination Deoxyribonucleic acid in eukaryotic cells is highly organized within the nucleus in the form of chromatin, a dynamic nucleoprotein complex whose fundamental structural unit is the nucleosome. The nucleosome consists of an octameric core formed by four pairs of histone proteins, namely H3, H4, H2A, and H2B. These histone proteins play a key role in chromatin organization and are subject to numerous post-translational modifications catalyzed by specialized histone- modifying enzymes. A wide spectrum of histone alteration has been identified, including methylation, acetylation, lactylation, phosphorylation, dopaminylation, and ubiquitination, among others, which collectively regulate chromatin structure and gene expression [1]. Aberrant regulation of histone methylation is associated with functional disturbances that contribute to the progression of numerous pathological conditions, including diabetes mellitus, arterial hypertension, atherosclerosis, fatty liver disease, malignancies, and autoimmune disorders [2]. In recent years, growing attention has been directed toward the involvement of histone methylation in the pathogenesis of MASLD. Experimental evidence indicates that elevated trimethylation at lysine 27 of histone H3 (H3K27me3) is associated with increased expression of genes involved in lipid biosynthesis. Enhancer of zeste homolog 2, a catalytic subunit of the polycomb repressive complex 2 and a key methyltransferase responsible for H3K27 methylation, has been shown to play a crucial role in regulating different phenotypic manifestations of MASLD by targeting distinct gene sets at various stages of disease progression [3].