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      Annexin A1 in the nervous and ocular systems

      review-article
      1 , 1 , , PhD 2 , * , , PhD 1 , *
      Neural Regeneration Research
      Wolters Kluwer - Medknow
      Annexin A1 (ANXA1), glaucoma, nervous system, neuroprotection, neuroregeneration, ocular disease, retina

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          Abstract

          The therapeutic potential of Annexin A1, an important member of the Annexin superfamily, has become evident in results of experiments with multiple human systems and animal models. The anti-inflammatory and pro-resolving effects of Annexin A1 are characteristic of pathologies involving the nervous system. In this review, we initially describe the expression sites of Annexin A1, then outline the mechanisms by which Annexin A1 maintains the neurological homeostasis through either formyl peptide receptor 2 or other molecular approaches; and, finally, we discuss the neuroregenerative potential qualities of Annexin A1. The eye and the nervous system are anatomically and functionally connected, but the association between visual system pathogenesis, especially in the retina, and Annexin A1 alterations has not been well summarized. Therefore, we explain the beneficial effects of Annexin A1 for ocular diseases, especially for retinal diseases and glaucoma on the basis of published findings, and we explore present and future delivery strategies for Annexin A1 to the retina.

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          Most cited references103

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          Microglia Function in the Central Nervous System During Health and Neurodegeneration.

          Microglia are resident cells of the brain that regulate brain development, maintenance of neuronal networks, and injury repair. Microglia serve as brain macrophages but are distinct from other tissue macrophages owing to their unique homeostatic phenotype and tight regulation by the central nervous system (CNS) microenvironment. They are responsible for the elimination of microbes, dead cells, redundant synapses, protein aggregates, and other particulate and soluble antigens that may endanger the CNS. Furthermore, as the primary source of proinflammatory cytokines, microglia are pivotal mediators of neuroinflammation and can induce or modulate a broad spectrum of cellular responses. Alterations in microglia functionality are implicated in brain development and aging, as well as in neurodegeneration. Recent observations about microglia ontogeny combined with extensive gene expression profiling and novel tools to study microglia biology have allowed us to characterize the spectrum of microglial phenotypes during development, homeostasis, and disease. In this article, we review recent advances in our understanding of the biology of microglia, their contribution to homeostasis, and their involvement in neurodegeneration. Moreover, we highlight the complexity of targeting microglia for therapeutic intervention in neurodegenerative diseases. Expected final online publication date for the Annual Review of Immunology Volume 35 is April 26, 2017. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.
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            A blood–brain barrier overview on structure, function, impairment, and biomarkers of integrity

            The blood–brain barrier is playing a critical role in controlling the influx and efflux of biological substances essential for the brain’s metabolic activity as well as neuronal function. Thus, the functional and structural integrity of the BBB is pivotal to maintain the homeostasis of the brain microenvironment. The different cells and structures contributing to developing this barrier are summarized along with the different functions that BBB plays at the brain–blood interface. We also explained the role of shear stress in maintaining BBB integrity. Furthermore, we elaborated on the clinical aspects that correlate between BBB disruption and different neurological and pathological conditions. Finally, we discussed several biomarkers that can help to assess the BBB permeability and integrity in-vitro or in-vivo and briefly explain their advantages and disadvantages.
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              Spinal Cord Injury: Pathophysiology, Multimolecular Interactions, and Underlying Recovery Mechanisms

              Spinal cord injury (SCI) is a destructive neurological and pathological state that causes major motor, sensory and autonomic dysfunctions. Its pathophysiology comprises acute and chronic phases and incorporates a cascade of destructive events such as ischemia, oxidative stress, inflammatory events, apoptotic pathways and locomotor dysfunctions. Many therapeutic strategies have been proposed to overcome neurodegenerative events and reduce secondary neuronal damage. Efforts have also been devoted in developing neuroprotective and neuro-regenerative therapies that promote neuronal recovery and outcome. Although varying degrees of success have been achieved, curative accomplishment is still elusive probably due to the complex healing and protective mechanisms involved. Thus, current understanding in this area must be assessed to formulate appropriate treatment modalities to improve SCI recovery. This review aims to promote the understanding of SCI pathophysiology, interrelated or interlinked multimolecular interactions and various methods of neuronal recovery i.e., neuroprotective, immunomodulatory and neuro-regenerative pathways and relevant approaches.
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                Author and article information

                Journal
                Neural Regen Res
                Neural Regen Res
                NRR
                Neural Regen Res
                Neural Regeneration Research
                Wolters Kluwer - Medknow (India )
                1673-5374
                1876-7958
                March 2024
                20 July 2023
                : 19
                : 3
                : 591-597
                Affiliations
                [1 ]Department of Ophthalmology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, China
                [2 ]Department of Anesthesiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, China
                Author notes
                [* ] Correspondence to: Xing Li, lixing88@ 123456hust.edu.cn ; Yin Zhao, zhaoyin85@ 123456hust.edu.cn .

                Author contributions: Writing original draft: AW; review & editing: HZ; supervision, resources, review & editing: XL and YZ. All approved the final version of the manuscript .

                Author information
                https://orcid.org/0000-0003-3462-7541
                https://orcid.org/0000-0002-1470-7184
                Article
                NRR-19-591
                10.4103/1673-5374.380882
                10581565
                37721289
                4c4746e7-f4b5-427d-a268-9d4657b4e3ce
                Copyright: © Neural Regeneration Research

                This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms.

                History
                : 15 February 2023
                : 06 May 2023
                : 02 June 2023
                Categories
                Review

                annexin a1 (anxa1),glaucoma,nervous system,neuroprotection,neuroregeneration,ocular disease,retina

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