期刊
PROCEEDINGS OF THE JAPAN ACADEMY SERIES B-PHYSICAL AND BIOLOGICAL SCIENCES
卷 88, 期 8, 页码 434-453出版社
JAPAN ACAD
DOI: 10.2183/pjab.88.434
关键词
ASK1; inhibitors; MAP kinase; signal transduction; stress
资金
- JSPS
- MEXT
- Global Center of Education and Research for Chemical Biology of the Diseases
- Naito Foundation Natural Science Scholarship
- Cosmetology Research Foundation
- Tokyo Biochemical Research Foundation
- Grants-in-Aid for Scientific Research [22390347, 24659027, 20229004, 23659033] Funding Source: KAKEN
Apoptosis signal-regulating kinase 1 (ASK1) is a member of the mitogen-activated protein kinase kinase kinase (MAP3K) family that activates downstream MAP kinases (MAPKs), c-Jun N-terminal kinases (JNKs) and p38 MAPKs, in response to various stresses, such as reactive oxygen species (ROS), endoplasmic reticulum (ER) stress, lipopolysaccharide, and calcium overload. Activation of the JNK and p38 pathways induces stress responses such as cell death, differentiation, and the production of inflammatory cytokines. A series of studies using ASK1-deficient mice have indicated that ASK1 plays important roles in many stress-related diseases, including cardiovascular and neurodegenerative diseases, suggesting that small compounds that inhibit ASK1 activity could possibly be used for the amelioration of the development and/or progression of these diseases. In this review, we provide an overview of the pathophysiological roles of ASK1-dependent signaling pathways and discuss the mechanistic basis for how these could serve as potential therapeutic targets.
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