Role and mechanisms of cytokines in the secondary brain injury after intracerebral hemorrhage

Huimin Zhu; Zhiqiang Wang; Jixu Yu; Xiuli Yang; Feng He; Zhenchuan Liu; Fengyuan Che; Xuemei Chen; Honglei Ren; Michael Hong; Jian Wang

doi:10.1016/j.pneurobio.2019.03.003

Role and mechanisms of cytokines in the secondary brain injury after intracerebral hemorrhage

Huimin Zhu, Zhiqiang Wang, Jixu Yu, Xiuli Yang, Feng He, Zhenchuan Liu, Fengyuan Che, Xuemei Chen, Honglei Ren, Michael Hong, Jian Wang

School of Medicine

Research output: Contribution to journal › Review article › peer-review

44 Scopus citations

Abstract

Intracerebral hemorrhage (ICH) is a common and severe cerebrovascular disease that has high mortality. Few survivors achieve self-care. Currently, patients receive only symptomatic treatment for ICH and benefit poorly from this regimen. Inflammatory cytokines are important participants in secondary injury after ICH. Increases in proinflammatory cytokines may aggravate the tissue injury, whereas increases in anti-inflammatory cytokines might be protective in the ICH brain. Inflammatory cytokines have been studied as therapeutic targets in a variety of acute and chronic brain diseases; however, studies on ICH are limited. This review summarizes the roles and functions of various pro- and anti-inflammatory cytokines in secondary brain injury after ICH and discusses pathogenic mechanisms and emerging therapeutic strategies and directions for treatment of ICH.

Original language	English (US)
Article number	101610
Journal	Progress in Neurobiology
Volume	178
DOIs	https://doi.org/10.1016/j.pneurobio.2019.03.003
State	Published - Jul 2019

Keywords

Cytokines
ICH
Inflammatory reaction
Secondary injury

ASJC Scopus subject areas

General Neuroscience

Access to Document

10.1016/j.pneurobio.2019.03.003

Cite this

@article{6e63d05c7d7d4ed8854d21d9c9809a09,

title = "Role and mechanisms of cytokines in the secondary brain injury after intracerebral hemorrhage",

abstract = "Intracerebral hemorrhage (ICH) is a common and severe cerebrovascular disease that has high mortality. Few survivors achieve self-care. Currently, patients receive only symptomatic treatment for ICH and benefit poorly from this regimen. Inflammatory cytokines are important participants in secondary injury after ICH. Increases in proinflammatory cytokines may aggravate the tissue injury, whereas increases in anti-inflammatory cytokines might be protective in the ICH brain. Inflammatory cytokines have been studied as therapeutic targets in a variety of acute and chronic brain diseases; however, studies on ICH are limited. This review summarizes the roles and functions of various pro- and anti-inflammatory cytokines in secondary brain injury after ICH and discusses pathogenic mechanisms and emerging therapeutic strategies and directions for treatment of ICH.",

keywords = "Cytokines, ICH, Inflammatory reaction, Secondary injury",

author = "Huimin Zhu and Zhiqiang Wang and Jixu Yu and Xiuli Yang and Feng He and Zhenchuan Liu and Fengyuan Che and Xuemei Chen and Honglei Ren and Michael Hong and Jian Wang",

note = "Publisher Copyright: {\textcopyright} 2019 Elsevier Ltd",

year = "2019",

month = jul,

doi = "10.1016/j.pneurobio.2019.03.003",

language = "English (US)",

volume = "178",

journal = "Progress in Neurobiology",

issn = "0301-0082",

publisher = "Elsevier Limited",

}

TY - JOUR

T1 - Role and mechanisms of cytokines in the secondary brain injury after intracerebral hemorrhage

AU - Zhu, Huimin

AU - Wang, Zhiqiang

AU - Yu, Jixu

AU - Yang, Xiuli

AU - He, Feng

AU - Liu, Zhenchuan

AU - Che, Fengyuan

AU - Chen, Xuemei

AU - Ren, Honglei

AU - Hong, Michael

AU - Wang, Jian

PY - 2019/7

Y1 - 2019/7

N2 - Intracerebral hemorrhage (ICH) is a common and severe cerebrovascular disease that has high mortality. Few survivors achieve self-care. Currently, patients receive only symptomatic treatment for ICH and benefit poorly from this regimen. Inflammatory cytokines are important participants in secondary injury after ICH. Increases in proinflammatory cytokines may aggravate the tissue injury, whereas increases in anti-inflammatory cytokines might be protective in the ICH brain. Inflammatory cytokines have been studied as therapeutic targets in a variety of acute and chronic brain diseases; however, studies on ICH are limited. This review summarizes the roles and functions of various pro- and anti-inflammatory cytokines in secondary brain injury after ICH and discusses pathogenic mechanisms and emerging therapeutic strategies and directions for treatment of ICH.

AB - Intracerebral hemorrhage (ICH) is a common and severe cerebrovascular disease that has high mortality. Few survivors achieve self-care. Currently, patients receive only symptomatic treatment for ICH and benefit poorly from this regimen. Inflammatory cytokines are important participants in secondary injury after ICH. Increases in proinflammatory cytokines may aggravate the tissue injury, whereas increases in anti-inflammatory cytokines might be protective in the ICH brain. Inflammatory cytokines have been studied as therapeutic targets in a variety of acute and chronic brain diseases; however, studies on ICH are limited. This review summarizes the roles and functions of various pro- and anti-inflammatory cytokines in secondary brain injury after ICH and discusses pathogenic mechanisms and emerging therapeutic strategies and directions for treatment of ICH.

KW - Cytokines

KW - ICH

KW - Inflammatory reaction

KW - Secondary injury

UR - http://www.scopus.com/inward/record.url?scp=85064458162&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85064458162&partnerID=8YFLogxK

U2 - 10.1016/j.pneurobio.2019.03.003

DO - 10.1016/j.pneurobio.2019.03.003

M3 - Review article

C2 - 30923023

AN - SCOPUS:85064458162

SN - 0301-0082

VL - 178

JO - Progress in Neurobiology

JF - Progress in Neurobiology

M1 - 101610

ER -

Role and mechanisms of cytokines in the secondary brain injury after intracerebral hemorrhage

Abstract

Keywords

ASJC Scopus subject areas

Access to Document

Other files and links

Fingerprint

Cite this