Scholarlink

<p>Apoptosis signal-regulating kinase 1 (ASK1) is a serine-threonine kinase, that is a member of the mitogen-activated protein kinase kinase (MAP3K) family, which is expressed or incorporated in nucleated cells which leads to the activation of multiple mitogen-activated protein kinases (MAPK) to regulate cell stress, tumour necrosis factor-α (TNF-α) ligand, lipopolysaccharides and apoptosis. ASK1 gets activated by the ROS, oxidative stress, endoplasmic stress (ER) and various inflammatory cytokines. Dysregulation of ASK1 can lead to various diseases like neurodegenerative disease, cardiovascular disease, cancer, and various other metabolic diseases such as diabetes. This review summarizes ASK1’s structure, its family, regulation, and its dual role in disease, highlighting its therapeutic potential for oxidative stress and inflammation-driven conditions while emphasizing the need for further clinical research. Inhibition of ASK1 demonstrates promising potential in treating fibrosis and various other diseases. We also discuss the dual role of ASK1 in both cancer initiation and suppression. Additionally, we explore ASK1 as a therapeutic target in diseases driven by oxidative stress and inflammation, emphasizing the need for further research to support its clinical translation.</p> Graphical abstract <p></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

Updated insights on ASK1 signaling: mechanisms, regulation, and therapeutic potential in diseases

  • 期刊论文

  • 发表日期：

    2025年6月14日

查看全文
  • Divyanshi Thakur,
  • Aniket Nandi,
  • Yash Kumar Gaur,
  • Karthikeyan Chandrabose,
  • Digambar Kumar Waiker,
  • Ghanshyam Das Gupta,
  • Kalicharan Sharma

摘要

Apoptosis signal-regulating kinase 1 (ASK1) is a serine-threonine kinase, that is a member of the mitogen-activated protein kinase kinase (MAP3K) family, which is expressed or incorporated in nucleated cells which leads to the activation of multiple mitogen-activated protein kinases (MAPK) to regulate cell stress, tumour necrosis factor-α (TNF-α) ligand, lipopolysaccharides and apoptosis. ASK1 gets activated by the ROS, oxidative stress, endoplasmic stress (ER) and various inflammatory cytokines. Dysregulation of ASK1 can lead to various diseases like neurodegenerative disease, cardiovascular disease, cancer, and various other metabolic diseases such as diabetes. This review summarizes ASK1’s structure, its family, regulation, and its dual role in disease, highlighting its therapeutic potential for oxidative stress and inflammation-driven conditions while emphasizing the need for further clinical research. Inhibition of ASK1 demonstrates promising potential in treating fibrosis and various other diseases. We also discuss the dual role of ASK1 in both cancer initiation and suppression. Additionally, we explore ASK1 as a therapeutic target in diseases driven by oxidative stress and inflammation, emphasizing the need for further research to support its clinical translation.

Graphical abstract