Scholarlink

<p>Cell migration, which is often impaired under high glucose (HG) conditions, plays a crucial role in the pathogenesis of various diabetic complications. This study investigates the role of mitochondrial aldehyde dehydrogenase (ALDH2) in the HG-induced migratory inhibition. Using fibroblasts sub-cultured in HG medium as a cell model of chronic hyperglycemia, we found that prolonged exposure to HG stress inhibited cell migration via a novel mechanism independent of oxidative stress or cell death. By increasing osmolality, HG induced perinuclear clustering of mitochondria, enhanced focal adhesion maturation, and caused the cells to be less responsive to migratory cues. The pharmacological inhibition of ALDH2 exaggerated this phenomenon, while ALDH2 overexpression protected cells from the migratory impairment caused by HG-induced hyperosmolality. Cells with ALDH2 overexpression exhibited less mature focal adhesions and longer mitochondrial network, suggesting that ALDH2 might preserve mitochondrial integrity to facilitate the focal adhesion turnover during cell migration.</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

Mitochondrial aldehyde dehydrogenase restores the migratory capacity inhibited by high glucose-induced hyperosmolality

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年5月22日

查看全文
  • Chi-Cheng Huang,
  • Yuh-Lien Chen,
  • Chung-Liang Chien

摘要

Cell migration, which is often impaired under high glucose (HG) conditions, plays a crucial role in the pathogenesis of various diabetic complications. This study investigates the role of mitochondrial aldehyde dehydrogenase (ALDH2) in the HG-induced migratory inhibition. Using fibroblasts sub-cultured in HG medium as a cell model of chronic hyperglycemia, we found that prolonged exposure to HG stress inhibited cell migration via a novel mechanism independent of oxidative stress or cell death. By increasing osmolality, HG induced perinuclear clustering of mitochondria, enhanced focal adhesion maturation, and caused the cells to be less responsive to migratory cues. The pharmacological inhibition of ALDH2 exaggerated this phenomenon, while ALDH2 overexpression protected cells from the migratory impairment caused by HG-induced hyperosmolality. Cells with ALDH2 overexpression exhibited less mature focal adhesions and longer mitochondrial network, suggesting that ALDH2 might preserve mitochondrial integrity to facilitate the focal adhesion turnover during cell migration.