• Special Issue Topic

    Therapeutic Targets for Neuroprotection in Ischemic Stroke

    Submission Deadline: August 31, 2024

    Guest Editor

    Dr. Silvia Fischer E-Mail

    Institute of Biochemistry, medicine, Justus-Liebig-University, Giessen, Germany

    Research Keywords: Endothelial cells; angiogenesis; endothelium; innate immunity; inflammatory responses

    About the Special Issue

    Stroke still belongs to the leading causes of death worldwide, accounting for 7.08 million deaths in 2020. Ischemic stroke is responsible for approximately 87% of all strokes, while hemorrhagic stroke accounts for 13%. Ischemic stroke, caused for example by thrombosis, embolism or systemic hypoperfusion, results in impaired blood flow and cell death, especially of neurons. Clinically, only intravenous thrombolysis with recombinant tissue plasminogen activator (rt-PA) and mechanical thrombectomy are administered for acute ischemic stroke to restore the blood flow. Unfortunately, both treatments are limited because of a very short therapeutic window and numerous contra-indications. Therefore, more knowledge about pathological cellular and molecular mechanisms in ischemic stroke is necessary to develop new strategies of neuroprotection. Some of the molecular events that can be targeted by neuroprotectants include glutamate release, glutamate receptor activation, intracellular Ca2+ increase, mitochondrial dysfunction, activation of several intracellular enzymes, generation of free radicals, apoptosis, blood-brain barrier disruption, and inflammation. Furthermore, ischemic stroke results in the release of danger associated molecular patterns (DAMPs) from dying cells such as heat shock proteins, histones, thioredoxin, adenosine triphosphate, high mobility group box protein 1, and numerous self-nucleic acids. These DAMPs can orchestrate innate and adaptive immune responses in the injured regions of the brain by glial cell activation, leading to the release of cytokines and chemokines, and the recruitment of leukocytes. Activated neutrophils further release neutrophil extracellular traps (NETs) which have been identified in infarcted lesions in specimens from ischemic stroke patients. Thus, inhibitory targeting of these events might provide promising therapeutic interventions to treat ischemic stroke.

    This special issue summarizes new knowledge about cellular and molecular mechanisms in ischemic stroke and treatment modalities.

    Keywords: ischemic stroke; neuroprotection; neurons; glial cells; danger-associated molecular patterns; inflammation

    Call for Papers

    Published Articles

    Open Access
    Advances in neuroprotective therapy for acute ischemic stroke
    Acute ischemic stroke (AIS) is the leading cause of disability worldwide, and recanalization therapy is primary in the hyperacute phase of AIS. However, reperfusion injury and hemorrhagic transforma [...] Read more.
    Yang Yang ... Yi Li
    Published: February 27, 2024 Explor Neuroprot Ther. 2024;4:55–71
    DOI: https://doi.org/10.37349/ent.2024.00070
    Times Cited: 0
    Open Access
    Efficacy and safety of CDP-choline, cerebrolysin, MLC601, and edaravone in recovery of patients with acute ischemic strokes: a meta-analysis
    Aim: Stroke is the second most common cause of mortality and disability worldwide with ischemic strokes being the predominant type. The advent of neuroprotectants brought hope of improved outcome [...] Read more.
    Shafiq Dexter B. Abou Zaki, Johnny K. Lokin
    Published: October 31, 2023 Explor Neuroprot Ther. 2023;3:398–408
    DOI: https://doi.org/10.37349/ent.2023.00057
    Open Access
    Stem cell therapy in neurological disorders: promises and concerns
    Self-neuronal regeneration is often limited or nonexistent after neuronal cell damage, making new technologies necessary for treating neurological damage. Although the brain can partially compensate [...] Read more.
    Said Hachimi-Idrissi
    Published: October 31, 2023 Explor Neuroprot Ther. 2023;3:346–362
    DOI: https://doi.org/10.37349/ent.2023.00055
    Times Cited: 0