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Updated: May 8, 2025

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Knockdown of RASD1 improves MASLD progression by inhibiting the PI3K/AKT/mTOR pathway

Guifang Zeng1, Xialei Liu2, Zhouying Zheng2

  • 1Department of Hepatobiliary Surgery, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, Guangdong, 519000, People's Republic of China. zenggf6@mail2.sysu.edu.cn.

Lipids in Health and Disease
|December 28, 2024
PubMed
Abstract

Insights

Ras-related dexamethasone-induced 1 (RASD1) is upregulated in metabolic dysfunction-associated steatotic liver disease (MASLD). Reducing RASD1 alleviates lipid deposition by inhibiting de novo lipogenesis, suggesting RASD1 as a potential therapeutic target for MASLD.

Area of Science:

  • Hepatology
  • Molecular Biology
  • Metabolic Disorders

Background:

  • Metabolic dysfunction-associated steatotic liver disease (MASLD) lacks effective treatments.
  • The role of Ras-related dexamethasone-induced 1 (RASD1) in MASLD pathogenesis is unclear.

Purpose of the Study:

  • To investigate the role of RASD1 in MASLD.
  • To elucidate the underlying mechanisms by which RASD1 affects MASLD.

Main Methods:

  • Validated RASD1 expression in MASLD models.
  • Investigated lipid metabolism in hepatocytes and mice with altered RASD1 levels (overexpression/knockdown).

Main Results:

  • RASD1 expression is elevated in MASLD.
  • RASD1 knockdown reduced lipid deposition and de novo lipogenesis gene expression.
  • RASD1 overexpression had opposite effects, indicating its role in lipid metabolism regulation via the PI3K/AKT/mTOR pathway.

Conclusions:

  • RASD1 plays a significant role in MASLD by promoting lipogenesis.
  • RASD1 regulates lipid metabolism through the PI3K/AKT/mTOR signaling pathway.
  • RASD1 represents a potential therapeutic target for MASLD treatment.
Keywords:
Lipid metabolismMASLDPI3K/AKT/mTOR pathwayRas-related dexamethasone-induced 1

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