Abstract
Aneurysmal subarachnoid hemorrhage (SAH) is known as one of the most devastating diseases in the central nervous system. In the past few decades, research on SAH has focused on cerebral vasospasm to prevent post-SAH delayed cerebral ischemia (DCI) and to improve outcomes. However, increasing evidence has suggested that early brain injury (EBI) is an important mechanism contributing to DCI, cerebral vasospasm as well as poor outcomes. Though the mechanism of EBI is very complex, inflammation is thought to play a pivotal role in EBI. Galectin-3 is a unique chimera type in the galectin family characterized by its β-galactoside-binding lectin, which mediates various pathologies, such as fibrosis, cell adhesion, and inflammation. Recently, two clinical studies revealed galectin-3 to be a possible prognostic biomarker in SAH patients. In addition, our recent report suggested that higher acute-stage plasma galectin-3 levels correlated with subsequent development of delayed cerebral infarction that was not associated with vasospasm in SAH patients. We review the possible role and molecular mechanisms of inflammation as well as galectin-3 in brain injuries, especially focusing on EBI after SAH, and discuss galectin-3 as a potential new therapeutic or research target in post-SAH brain injuries.
Highlights
Subarachnoid hemorrhage (SAH) by rupture of cerebral aneurysm is an important cause of stroke mortality and morbidity [1]
Recent studies have shown that the inflammatory response, including glial cell activation, contributes to early brain injury (EBI) and delayed cerebral ischemia due to cerebral vasospasm and/or other etiologies, causing poor outcomes after SAH [1]
After SAH, blood components including heme, thrombin, platelets and leukocytes activate microglia, the frontline soldiers of immune defense in the central nervous system (CNS), which serve as tissue-resident macrophages and produce pro-inflammatory cytokines and galectin-3 [1,2]
Summary
Subarachnoid hemorrhage (SAH) by rupture of cerebral aneurysm is an important cause of stroke mortality and morbidity [1]. After SAH, blood components including heme, thrombin, platelets and leukocytes activate microglia, the frontline soldiers of immune defense in the central nervous system (CNS), which serve as tissue-resident macrophages and produce pro-inflammatory cytokines and galectin-3 [1,2]. Matricellular proteins, such as galectin-3, tenascin-C (TNC) and osteopontin, have garnered significant attention as biomarkers for various diseases [2,3,4]. This review focuses on possible roles of galectin-3 in brain injuries after SAH, relevant to inflammation and microglia
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