期刊
JOURNAL OF ADVANCED RESEARCH
卷 54, 期 -, 页码 43-57出版社
ELSEVIER
DOI: 10.1016/j.jare.2023.01.020
关键词
Nischarin/IRAS; Neurodevelopment; Spinal cord injury; Opioid dependence; Anxiety; Depression; Autism
This review systematically analyzes the role and mechanism of Nischarin/IRAS in the CNS, providing necessary references and potential treatment targets for neurological diseases, thereby expanding the direction of Nischarin/IRAS research and facilitating clinical translation.
Background: Murine Nischarin and its human homolog IRAS are scaffold proteins highly expressed in the central nervous system (CNS). Nischarin was initially discovered as a tumor suppressor protein, and recent studies have also explored its potential value in the CNS. Research on IRAS has largely focused on its effect on opioid dependence. Although the role of Nischarin/IRAS in the physiological function and pathological process of the CNS has gradually attracted attention and the related research results are expected to be applied in clinical practice, there is no systematic review of the role and mechanisms of Nischarin/IRAS in the CNS so far.Aim of review: This review will systematically analyze the role and mechanism of Nischarin/IRAS in the CNS, and provide necessary references and possible targets for the treatment of neurological diseases, thereby broadening the direction of Nischarin/IRAS research and facilitating clinical translation.Key scientific concepts of review: The pathophysiological processes affected by dysregulation of Nischarin/ IRAS expression in the CNS are mainly introduced, including spinal cord injury (SCI), opioid dependence, anxiety, depression, and autism. The molecular mechanisms such as factors regulating Nischarin/IRAS expression and signal transduction pathways regulated by Nischarin/IRAS are systematically summa-rized. Finally, the clinical application of Nischarin/IRAS has been prospected.(c) 2023 The Authors. Published by Elsevier B.V. on behalf of Cairo University. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
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