Abstract
Despite years of encouraging translational research, ischemic stroke still remains as one of the highest unmet medical needs nowadays, causing a tremendous burden to health care systems worldwide. Following an ischemic insult, a complex signaling pathway emerges leading to highly interconnected thrombotic as well as neuroinflammatory signatures, the so-called thromboinflammatory cascade. Here, we thoroughly review the cell-specific and time-dependent role of different immune cell types, i.e., neutrophils, macrophages, T and B cells, as key thromboinflammatory mediators modulating the neuroinflammatory response upon stroke. Similarly, the relevance of platelets and their tight crosstalk with a variety of immune cells highlights the relevance of this cell-cell interaction during microvascular dysfunction, neovascularization, and cellular adhesion. Ultimately, we provide an up-to-date overview of therapeutic approaches mechanistically targeting thromboinflammation currently under clinical translation, especially focusing on phase I to III clinical trials.
Original language | English |
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Pages (from-to) | 389-410 |
Number of pages | 22 |
Journal | Seminars in Immunopathology |
Volume | 45 |
Issue number | 3 |
DOIs | |
Publication status | Published - 1 May 2023 |
Keywords
- Brain ischemia
- Thromboinflammation
- Stroke recovery
- Platelet
- Neuroinflammation
- ACUTE ISCHEMIC-STROKE
- REGULATORY T-CELLS
- INTERCELLULAR-ADHESION MOLECULE-1
- PLASMINOGEN-ACTIVATOR INHIBITOR-1
- P-SELECTIN
- GLYCOPROTEIN-VI
- BRAIN-INJURY
- PLATELET-ADHESION
- NEUTROPHIL RECRUITMENT
- COGNITIVE IMPAIRMENT