Scholarlink

<p>Metabolic dysfunction-associated steatohepatitis (MASH) has become a major global health issue. Mitochondrial damage plays a crucial role in the development and progression of MASH. Therefore, it is speculated that mitochondrial transplantation therapy, which could replace dysfunctional mitochondria with normal ones, might potentially restore the liver cell metabolism of MASH. In palmitate-damaged AML-12 hepatocytes, exogenous mitochondria could eliminate lipid deposits and recover cell viability. However, in transforming growth factor β (TGF-β)-activated hepatic stellate cells (HSCs), the exogenous mitochondria showed the capability to inhibit the generation of α-smooth muscle actin (α-SMA) and collagen I. Moreover, the mechanism by which the exogenous mitochondria initiated the mitochondria-nucleus signaling pathway of liver cells was studied. The results showed the mitochondria could prevent metabolism disorders in the liver cells by regulating silent information regulator 1 (SIRT1) activity. Subsequently, a MASH animal model was established by the administration of a high-fat diet and the intraperitoneal injection of carbon tetrachloride to Kunming mice. The results indicated that the mitochondrial therapy significantly inhibited the livery injury and restored liver cell function in the experimental MASH mice (<i>p</i> &lt; 0.01). The mitochondrial therapy would be a promising strategy to improve MASH pathological features, which could be developed as a new treatment option against MASH.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Healthy mitochondria attenuate metabolic dysfunction-associated steatohepatitis by restoring cell metabolism

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年10月11日

查看全文
  • Peiyu Zhou,
  • Jingli Li,
  • Yafang Xie,
  • Xiaorong Li,
  • Zhihong Cui,
  • Ailing Fu

摘要

Metabolic dysfunction-associated steatohepatitis (MASH) has become a major global health issue. Mitochondrial damage plays a crucial role in the development and progression of MASH. Therefore, it is speculated that mitochondrial transplantation therapy, which could replace dysfunctional mitochondria with normal ones, might potentially restore the liver cell metabolism of MASH. In palmitate-damaged AML-12 hepatocytes, exogenous mitochondria could eliminate lipid deposits and recover cell viability. However, in transforming growth factor β (TGF-β)-activated hepatic stellate cells (HSCs), the exogenous mitochondria showed the capability to inhibit the generation of α-smooth muscle actin (α-SMA) and collagen I. Moreover, the mechanism by which the exogenous mitochondria initiated the mitochondria-nucleus signaling pathway of liver cells was studied. The results showed the mitochondria could prevent metabolism disorders in the liver cells by regulating silent information regulator 1 (SIRT1) activity. Subsequently, a MASH animal model was established by the administration of a high-fat diet and the intraperitoneal injection of carbon tetrachloride to Kunming mice. The results indicated that the mitochondrial therapy significantly inhibited the livery injury and restored liver cell function in the experimental MASH mice (p < 0.01). The mitochondrial therapy would be a promising strategy to improve MASH pathological features, which could be developed as a new treatment option against MASH.