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Journal ArticleDOI

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

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TLDR
A 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.
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This article is published in Progress in Neurobiology.The article was published on 2019-07-01. It has received 162 citations till now. The article focuses on the topics: Proinflammatory cytokine & Intracerebral hemorrhage.

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Caspase-1-induced pyroptosis is an innate immune effector mechanism against intracellular bacteria (111.33)

TL;DR: It is demonstrated that activation of caspase-1 clears intracellular bacteria in vivo independently of IL-1β and IL-18 and establishes pyroptosis as an efficient mechanism of bacterial clearance by the innate immune system.
Journal ArticleDOI

Neuroinflammation in intracerebral haemorrhage: immunotherapies with potential for translation.

TL;DR: The quick initiation of these drugs, particularly in high systemic doses, could be key to counteracting the evolving secondary injury in people with intracerebral haemorrhage and provides a promising way in which the poor prognosis of intrACErebralHaemorhage might one day be counteracted.
Journal ArticleDOI

Potential therapeutic targets for intracerebral hemorrhage-associated inflammation: An update

TL;DR: An update of recent progress on ICH is provided and the prospects for further preclinical studies in this field are described and new therapeutic targets and directions for the treatment of ICH are discussed.
Journal ArticleDOI

Pathophysiological Mechanisms and Potential Therapeutic Targets in Intracerebral Hemorrhage.

TL;DR: Some key pathophysiology mechanisms in ICH such as oxidative stress, inflammation, iron toxicity, and thrombin formation are discussed and the corresponding therapeutic targets and therapeutic strategies are reviewed.
Journal ArticleDOI

Recombinant Adiponectin Peptide Ameliorates Brain Injury Following Intracerebral Hemorrhage by Suppressing Astrocyte-Derived Inflammation via the Inhibition of Drp1-Mediated Mitochondrial Fission.

TL;DR: First mechanistic evidence is provided that APNp can modulate Drp1-mediated mitochondrial fission, which then contributes to alleviating astrocyte-derived inflammation, ultimately attenuating inflammatory brain injury induced by hemorrhage.
References
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Journal ArticleDOI

Global, regional, and national age-sex specific all-cause and cause-specific mortality for 240 causes of death, 1990-2013: A systematic analysis for the Global Burden of Disease Study 2013

Mohsen Naghavi, +731 more
- 10 Jan 2015 - 
TL;DR: In the Global Burden of Disease Study 2013 (GBD 2013) as discussed by the authors, the authors used the GBD 2010 methods with some refinements to improve accuracy applied to an updated database of vital registration, survey, and census data.
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IL-23 drives a pathogenic T cell population that induces autoimmune inflammation

TL;DR: Using passive transfer studies, it is confirmed that these IL-23–dependent CD4+ T cells are highly pathogenic and essential for the establishment of organ-specific inflammation associated with central nervous system autoimmunity.
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Interleukin 10(IL-10) inhibits cytokine synthesis by human monocytes: an autoregulatory role of IL-10 produced by monocytes.

TL;DR: The results indicate that IL-10 has important regulatory effects on immunological and inflammatory responses because of its capacity to downregulate class II MHC expression and to inhibit the production of proinflammatory cytokines by monocytes.
Journal ArticleDOI

Bcl-2 antiapoptotic proteins inhibit Beclin 1-dependent autophagy.

TL;DR: Bcl-2 not only functions as an antiapoptotic protein, but also as an antiautophagy protein via its inhibitory interaction with Beclin 1, which may help maintain autophagy at levels that are compatible with cell survival, rather than cell death.
Journal ArticleDOI

IL-33, an interleukin-1-like cytokine that signals via the IL-1 receptor-related protein ST2 and induces T helper type 2-associated cytokines

TL;DR: A member of theIL-1 family, IL-33, which mediates its biological effects via IL-1 receptor ST 2, activates NF-kappaB and MAP kinases, and drives production of T(H)2-associated cytokines from in vitro polarized T( H)2 cells is reported.
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