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Purpose of Review <p>This review explores the metabolic pathways dysregulated in both atherosclerotic cardiovascular disease (ASCVD) and metabolic dysfunction-associated steatotic liver disease (MASLD), focusing on lipid, carbohydrate, amino acid, and energy metabolism and the specific alterations within major contributing cell types.</p> Recent Findings <p>In the setting of metabolic syndrome, lipid and carbohydrate overload impair hepatic metabolism, resulting in the accumulation of lipotoxic species and ensuing cellular damage, inflammation, oxidative stress, and cardiovascular consequences. Amino acid metabolism is emerging as a key regulator of cell fate and function in both MASLD and ASCVD. Mitochondrial dysfunction and cellular stress promote a pseudo-Warburg effect, shifting cells from efficient oxidative phosphorylation to anaerobic glycolysis and impairing homeostasis. Emerging therapies targeting hepatic metabolism to reduce cardiovascular risk and MASLD burden hold promise for future dual treatments.</p> Summary <p>MASLD and ASCVD arise from common metabolic derangements that converge on shared cellular and molecular pathways. Defining these cross-tissue mechanisms may enable the development of integrated therapeutic approaches aimed at jointly mitigating hepatic and vascular injury, thus redefining treatment paradigms in cardiometabolic disease.</p>

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Metabolic Pathways Linking Atherosclerotic Cardiovascular Disease With Metabolic Dysfunction-Associated Steatotic Liver Disease

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年5月13日

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  • Koral S. E. Richard,
  • Sumati Rohilla,
  • Reethika Gade,
  • Fabio Arias,
  • Oren Rom

摘要

Purpose of Review

This review explores the metabolic pathways dysregulated in both atherosclerotic cardiovascular disease (ASCVD) and metabolic dysfunction-associated steatotic liver disease (MASLD), focusing on lipid, carbohydrate, amino acid, and energy metabolism and the specific alterations within major contributing cell types.

Recent Findings

In the setting of metabolic syndrome, lipid and carbohydrate overload impair hepatic metabolism, resulting in the accumulation of lipotoxic species and ensuing cellular damage, inflammation, oxidative stress, and cardiovascular consequences. Amino acid metabolism is emerging as a key regulator of cell fate and function in both MASLD and ASCVD. Mitochondrial dysfunction and cellular stress promote a pseudo-Warburg effect, shifting cells from efficient oxidative phosphorylation to anaerobic glycolysis and impairing homeostasis. Emerging therapies targeting hepatic metabolism to reduce cardiovascular risk and MASLD burden hold promise for future dual treatments.

Summary

MASLD and ASCVD arise from common metabolic derangements that converge on shared cellular and molecular pathways. Defining these cross-tissue mechanisms may enable the development of integrated therapeutic approaches aimed at jointly mitigating hepatic and vascular injury, thus redefining treatment paradigms in cardiometabolic disease.