Endoplasmic reticulum stress,autophagy,neuroinflammation,and sigma 1 receptors as contributors to depression and its treatment
Chika Fujii1
Charles F.Zorumski2
Yukitoshi Izumi2
1.Department of Psychiatry,Washington University School of Medicine,St.Louis,MO,USA2.Department of Psychiatry,Washington University School of Medicine,St.Louis,MO,USA;Taylor Family Institute for Innovative Psychiatric Research,Washington University School of Medicine,St.Louis,MO,USA
摘要：The etiological factors contributing to depression and other neuropsychiatric disorders are largely undefined.Endoplasmic reticulum stress pathways and autophagy are well-defined mechanisms that play critical functions in recognizing and resolving cellular stress and are possible targets for the pathophysiology and treatment of psychiatric and neurologic illnesses.An increasing number of studies indicate the involvement of endoplasmic reticulum stress and autophagy in the control of neuroinflammation,a contributing factor to multiple neuropsychiatric illnesses.Initial inflammatory triggers induce endoplasmic reticulum stress,leading to neuroinflammatory responses.Subsequently,induction of autophagy by neurosteroids and other signaling pathways that converge on autophagy induction are thought to participate in resolving neuroinflammation.The aim of this review is to summarize our current understanding of the molecular mechanisms governing the induction of endoplasmic reticulum stress,autophagy,and neuroinflammation in the central nervous system.Studies focused on innate immune factors,including neurosteroids with anti-inflammatory roles will be reviewed.In the context of depression,animal models that led to our current understanding of molecular mechanisms underlying depression will be highlighted,including the roles of sigma 1 receptors and pharmacological agents that dampen endoplasmic reticulum stress and associated neuroinflammation.
机标关键词：depressionstresssigmaautophagycontributorsendoplasmiceuroinflammation
论文发表日期：2024-10-28
在线出版日期：2025-08-15（本平台首次上网日期，不代表文献的发表时间）
页数：10( 2202-2211 )
英文信息