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Purpose of the Review <p>Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) is rapidly being recognized as a world health crisis, touching nearly a third of the world’s population. A key step in the progression of MASLD from simple steatosis to full-blown fibrosis is the unregulated lipid metabolism of the liver, especially the overexpression of <i>de novo</i> lipogenesis (DNL). This article aims to explore the relationship between m6A remodeling pathways and DNL in MASLD pathogenesis. It also addresses the therapeutic implications including both synthetic and natural products of these regulators towards managing MASLD by means of epitranscriptomic profiling.</p> Major Findings <p>Studies have identified RNA methylation in the form of N-6 Methyladenosine (m6A) as the master regulator of this unregulated lipid metabolism. It incorporates different regulators, termed writers, erasers, and readers, which determine the fate of lipid metabolism regulator transcripts. In MASLD, these regulators have been found to be compromised, especially in instances where the regulators expression are altered which results in the stabilization of lipid regulators such as SREBP-1c, FASN etc. However, of specific interest is the fact that m6A regulators are connected not only to lipid synthesis but also integrate signals of insulin resistance, oxidative stress, and mitochondrial dysfunction.</p> Summary <p>The recent emergence of epitranscriptomics has revolutionized our understanding of MASLD by revealing m6A methylation as a master regulator of DNL. The complex interplay between writers, erasers, and readers has established a highly complex post-transcriptional regulatory circuit that modulates the stability, export, and translation of primary lipogenic enzymes and transcription factors. The integration of epitranscriptomic profiling with current clinical diagnostic tools may, in the future, provide the means for personalized medicine strategies to be employed for the accurate treatment of MASLD according to the individual’s specific molecular profile. In the end, the connection between epitranscriptomic principles and clinical translation has the potential to turn MASLD from a global health crisis into a manageable disease.</p>

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Epitranscriptomic Remodeling: m6A Methylation as a Master Regulator of de novo Lipogenesis in MASLD

  • 期刊论文

  • 发表日期：

    2026年7月17日

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  • Pervej Alom Barbhuiya,
  • Pompy Patowary,
  • Manash Pratim Pathak

摘要

Purpose of the Review

Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) is rapidly being recognized as a world health crisis, touching nearly a third of the world’s population. A key step in the progression of MASLD from simple steatosis to full-blown fibrosis is the unregulated lipid metabolism of the liver, especially the overexpression of de novo lipogenesis (DNL). This article aims to explore the relationship between m6A remodeling pathways and DNL in MASLD pathogenesis. It also addresses the therapeutic implications including both synthetic and natural products of these regulators towards managing MASLD by means of epitranscriptomic profiling.

Major Findings

Studies have identified RNA methylation in the form of N-6 Methyladenosine (m6A) as the master regulator of this unregulated lipid metabolism. It incorporates different regulators, termed writers, erasers, and readers, which determine the fate of lipid metabolism regulator transcripts. In MASLD, these regulators have been found to be compromised, especially in instances where the regulators expression are altered which results in the stabilization of lipid regulators such as SREBP-1c, FASN etc. However, of specific interest is the fact that m6A regulators are connected not only to lipid synthesis but also integrate signals of insulin resistance, oxidative stress, and mitochondrial dysfunction.

Summary

The recent emergence of epitranscriptomics has revolutionized our understanding of MASLD by revealing m6A methylation as a master regulator of DNL. The complex interplay between writers, erasers, and readers has established a highly complex post-transcriptional regulatory circuit that modulates the stability, export, and translation of primary lipogenic enzymes and transcription factors. The integration of epitranscriptomic profiling with current clinical diagnostic tools may, in the future, provide the means for personalized medicine strategies to be employed for the accurate treatment of MASLD according to the individual’s specific molecular profile. In the end, the connection between epitranscriptomic principles and clinical translation has the potential to turn MASLD from a global health crisis into a manageable disease.