Mechanisms and Therapeutic Targets of Depression After Intracerebral Hemorrhage

The relationship between depression and intracerebral hemorrhage (ICH) is complicated. One of the most common neuropsychiatric comorbidities of hemorrhagic stroke is Post-ICH depression. Depression, as a neuropsychiatric symptom, also negatively impacts the outcome of ICH by enhancing morbidity, dis...

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Main Authors: Yinan Wu, Liangliang Wang, Kaimin Hu, Chengcheng Yu, Yuanhan Zhu, Suzhan Zhang, Anwen Shao
Format: Article
Language:English
Published: Frontiers Media S.A. 2018-12-01
Series:Frontiers in Psychiatry
Subjects:
Online Access:https://www.frontiersin.org/article/10.3389/fpsyt.2018.00682/full
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author Yinan Wu
Liangliang Wang
Kaimin Hu
Chengcheng Yu
Yuanhan Zhu
Suzhan Zhang
Anwen Shao
author_facet Yinan Wu
Liangliang Wang
Kaimin Hu
Chengcheng Yu
Yuanhan Zhu
Suzhan Zhang
Anwen Shao
author_sort Yinan Wu
collection DOAJ
description The relationship between depression and intracerebral hemorrhage (ICH) is complicated. One of the most common neuropsychiatric comorbidities of hemorrhagic stroke is Post-ICH depression. Depression, as a neuropsychiatric symptom, also negatively impacts the outcome of ICH by enhancing morbidity, disability, and mortality. However, the ICH outcome can be improved by antidepressants such as the frequently-used selective serotonin reuptake inhibitors. This review therefore presents the mechanisms of post-ICH depression, we grouped the mechanisms according to inflammation, oxidative stress (OS), apoptosis and autophagy, and explained them through their several associated signaling pathways. Inflammation is mainly related to Toll-like receptors (TLRs), the NF-kB mediated signal pathway, the PPAR-γ-dependent pathway, as well as other signaling pathways. OS is associated to nuclear factor erythroid-2 related factor 2 (Nrf2), the PI3K/Akt pathway and the MAPK/P38 pathway. Moreover, autophagy is associated with the mTOR signaling cascade and the NF-kB mediated signal pathway, while apoptosis is correlated with the death receptor-mediated apoptosis pathway, mitochondrial apoptosis pathway, caspase-independent pathways and others. Furthermore, we found that neuroinflammation, oxidative stress, autophagy, and apoptosis experience interactions with one another. Additionally, it may provide several potential therapeutic targets for patients that might suffer from depression after ICH.
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spelling doaj.art-37ccfec5a3004c88a9783985543623932022-12-21T18:35:55ZengFrontiers Media S.A.Frontiers in Psychiatry1664-06402018-12-01910.3389/fpsyt.2018.00682430842Mechanisms and Therapeutic Targets of Depression After Intracerebral HemorrhageYinan Wu0Liangliang Wang1Kaimin Hu2Chengcheng Yu3Yuanhan Zhu4Suzhan Zhang5Anwen Shao6Cancer Institute, Key Laboratory of Cancer Prevention and Intervention, China National Ministry of Education, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, ChinaInterdisciplinary Institute of Neuroscience and Technology, Qiushi Academy for Advanced Studies, Zhejiang University, Hangzhou, ChinaDepartment of Surgical Oncology, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, ChinaDepartment of Orthopedics, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, ChinaDepartment of Neurosurgery, Rongjun Hospital, Jiaxing, ChinaDepartment of Surgical Oncology, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, ChinaDepartment of Neurosurgery, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, ChinaThe relationship between depression and intracerebral hemorrhage (ICH) is complicated. One of the most common neuropsychiatric comorbidities of hemorrhagic stroke is Post-ICH depression. Depression, as a neuropsychiatric symptom, also negatively impacts the outcome of ICH by enhancing morbidity, disability, and mortality. However, the ICH outcome can be improved by antidepressants such as the frequently-used selective serotonin reuptake inhibitors. This review therefore presents the mechanisms of post-ICH depression, we grouped the mechanisms according to inflammation, oxidative stress (OS), apoptosis and autophagy, and explained them through their several associated signaling pathways. Inflammation is mainly related to Toll-like receptors (TLRs), the NF-kB mediated signal pathway, the PPAR-γ-dependent pathway, as well as other signaling pathways. OS is associated to nuclear factor erythroid-2 related factor 2 (Nrf2), the PI3K/Akt pathway and the MAPK/P38 pathway. Moreover, autophagy is associated with the mTOR signaling cascade and the NF-kB mediated signal pathway, while apoptosis is correlated with the death receptor-mediated apoptosis pathway, mitochondrial apoptosis pathway, caspase-independent pathways and others. Furthermore, we found that neuroinflammation, oxidative stress, autophagy, and apoptosis experience interactions with one another. Additionally, it may provide several potential therapeutic targets for patients that might suffer from depression after ICH.https://www.frontiersin.org/article/10.3389/fpsyt.2018.00682/fullintracerebral hemorrhagedepressioninflammationoxidative stressapoptosisreview
spellingShingle Yinan Wu
Liangliang Wang
Kaimin Hu
Chengcheng Yu
Yuanhan Zhu
Suzhan Zhang
Anwen Shao
Mechanisms and Therapeutic Targets of Depression After Intracerebral Hemorrhage
Frontiers in Psychiatry
intracerebral hemorrhage
depression
inflammation
oxidative stress
apoptosis
review
title Mechanisms and Therapeutic Targets of Depression After Intracerebral Hemorrhage
title_full Mechanisms and Therapeutic Targets of Depression After Intracerebral Hemorrhage
title_fullStr Mechanisms and Therapeutic Targets of Depression After Intracerebral Hemorrhage
title_full_unstemmed Mechanisms and Therapeutic Targets of Depression After Intracerebral Hemorrhage
title_short Mechanisms and Therapeutic Targets of Depression After Intracerebral Hemorrhage
title_sort mechanisms and therapeutic targets of depression after intracerebral hemorrhage
topic intracerebral hemorrhage
depression
inflammation
oxidative stress
apoptosis
review
url https://www.frontiersin.org/article/10.3389/fpsyt.2018.00682/full
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