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Molecular functions of ASK family in diseases caused by stress-induced inflammation and apoptosis
Kazuki Kojima1, Hidenori Ichijo1, Isao Naguro1
1Laboratory of Cell Signaling, Graduate School of Pharmaceutical Sciences, The University of Tokyo, 7-3-1, Hongo, Bunkyo-ku, Tokyo 113-0033, Japan.
Abstract:
VCells are constantly exposed to various types of stress, and disruption of the proper response leads to a variety of diseases. Among them, inflammation and apoptosis are important examples of critical responses and should be tightly regulated, as inappropriate control of these responses is detrimental to the organism. In several disease states, these responses are abnormally regulated, with adverse effects. Apoptosis signal-regulating kinase (ASK) family members are stress-responsive kinases that regulate inflammation and apoptosis after a variety of stimuli, such as oxidative stress and endoplasmic reticulum stress. In this review, we summarize recent reports on the ASK family in terms of their involvement in inflammatory diseases, focussing on upstream stimuli that regulate ASK family members.
Insights
Cellular stress triggers critical responses like inflammation and apoptosis. This review highlights how Apoptosis Signal-Regulating Kinase (ASK) family members regulate these processes and their role in inflammatory diseases.
Area of Science:
- Cellular biology
- Molecular mechanisms of disease
- Stress response pathways
Background:
- Cellular stress disrupts essential processes, leading to diseases.
- Inflammation and apoptosis are critical cellular responses that require tight regulation.
- Dysregulation of these responses contributes to various pathological conditions.
Purpose of the Study:
- To review the role of the Apoptosis Signal-Regulating Kinase (ASK) family in inflammatory diseases.
- To focus on the upstream stimuli that modulate ASK family member activity.
- To provide insights into the molecular regulation of stress responses.
Main Methods:
- Literature review of recent reports on ASK family kinases.
- Analysis of studies investigating stress stimuli (e.g., oxidative stress, ER stress).
- Examination of the link between ASK family members and inflammatory disease pathogenesis.
Main Results:
- ASK family members are key regulators of inflammation and apoptosis.
- Various stress stimuli, including oxidative and endoplasmic reticulum stress, activate ASK pathways.
- Aberrant regulation of ASK signaling is implicated in the development of inflammatory diseases.
Conclusions:
- The ASK family plays a crucial role in mediating cellular responses to stress.
- Understanding ASK regulation is vital for developing therapeutic strategies for inflammatory diseases.
- Further research into upstream stimuli controlling ASK activity is warranted.
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