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      Effects of ischemic postconditioning and long non-coding RNAs in ischemic stroke

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          ABSTRACT

          Stroke is a main cause of disability and death among adults in China, and acute ischemic stroke accounts for 80% of cases. The key to ischemic stroke treatment is to recanalize the blocked blood vessels. However, more than 90% of patients cannot receive effective treatment within an appropriate time, and delayed recanalization of blood vessels causes reperfusion injury. Recent research has revealed that ischemic postconditioning has a neuroprotective effect on the brain, but the mechanism has not been fully clarified. Long non-coding RNAs (lncRNAs) have previously been associated with ischemic reperfusion injury in ischemic stroke. LncRNAs regulate important cellular and molecular events through a variety of mechanisms, but a comprehensive analysis of potential lncRNAs involved in the brain protection produced by ischemic postconditioning has not been conducted. In this review, we summarize the common mechanisms of cerebral injury in ischemic stroke and the effect of ischemic postconditioning, and we describe the potential mechanisms of some lncRNAs associated with ischemic stroke.

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          Most cited references139

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          Heart Disease and Stroke Statistics—2016 Update

          Circulation, 133(4)
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            Long non-coding RNAs: new players in cell differentiation and development.

            Genomes of multicellular organisms are characterized by the pervasive expression of different types of non-coding RNAs (ncRNAs). Long ncRNAs (lncRNAs) belong to a novel heterogeneous class of ncRNAs that includes thousands of different species. lncRNAs have crucial roles in gene expression control during both developmental and differentiation processes, and the number of lncRNA species increases in genomes of developmentally complex organisms, which highlights the importance of RNA-based levels of control in the evolution of multicellular organisms. In this Review, we describe the function of lncRNAs in developmental processes, such as in dosage compensation, genomic imprinting, cell differentiation and organogenesis, with a particular emphasis on mammalian development.
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              Neuroinflammation: friend and foe for ischemic stroke

              Stroke, the third leading cause of death and disability worldwide, is undergoing a change in perspective with the emergence of new ideas on neurodegeneration. The concept that stroke is a disorder solely of blood vessels has been expanded to include the effects of a detrimental interaction between glia, neurons, vascular cells, and matrix components, which is collectively referred to as the neurovascular unit. Following the acute stroke, the majority of which are ischemic, there is secondary neuroinflammation that both promotes further injury, resulting in cell death, but conversely plays a beneficial role, by promoting recovery. The proinflammatory signals from immune mediators rapidly activate resident cells and influence infiltration of a wide range of inflammatory cells (neutrophils, monocytes/macrophages, different subtypes of T cells, and other inflammatory cells) into the ischemic region exacerbating brain damage. In this review, we discuss how neuroinflammation has both beneficial as well as detrimental roles and recent therapeutic strategies to combat pathological responses. Here, we also focus on time-dependent entry of immune cells to the ischemic area and the impact of other pathological mediators, including oxidative stress, excitotoxicity, matrix metalloproteinases (MMPs), high-mobility group box 1 (HMGB1), arachidonic acid metabolites, mitogen-activated protein kinase (MAPK), and post-translational modifications that could potentially perpetuate ischemic brain damage after the acute injury. Understanding the time-dependent role of inflammatory factors could help in developing new diagnostic, prognostic, and therapeutic neuroprotective strategies for post-stroke inflammation.
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                Author and article information

                Journal
                Bioengineered
                Bioengineered
                Bioengineered
                Taylor & Francis
                2165-5979
                2165-5987
                24 November 2022
                2022
                24 November 2022
                : 13
                : 6
                : 14799-14814
                Affiliations
                [a ]Institute of Neuroscience, Faculty of Basic Medical Science, Kunming Medical University; , Kunming, China
                [b ]Second Department of General Surgery, First People’s Hospital of Yunnan Province; , Kunming, China
                Author notes
                CONTACT Liyan Li kmliyanl@ 123456163.com Institute of Neurosicence, Faculty of Basic Medical Science, Kunming Medical University; , Kunming 650500, Yunnan, China
                Jianhui Guo guojianhuikm@ 123456163.com Second Department of General Surgery, First People’s Hospital of Yunnan Province; , Kunming 650034, Yunnan, China
                [#]

                Both authors contributed equally to this paper.

                Author information
                https://orcid.org/0000-0002-2411-4235
                Article
                2108266
                10.1080/21655979.2022.2108266
                9704383
                36420646
                2b32e1a5-d6ad-4694-8a06-c66eda5177c8
                © 2022 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Page count
                Figures: 0, Tables: 3, References: 139, Pages: 16
                Categories
                Review Article
                Review

                Biomedical engineering
                ischemic stroke,ischemic postconditioning,remote ischemic postconditioning,long non-coding rnas,neuroprotective effect

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