Abstract
Subarachnoid hemorrhage resulting from intracranial aneurysms (IAs) is associated with high rates of morbidity and mortality. Although trigger mechanisms in the pathogenesis of IAs have not been fully elucidated, accumulating evidence has demonstrated that inflammation acts as a critical contributor to aneurysm pathogenesis. IAs is initiated by disruption and dysfunction of endothelial cells (ECs) caused by abnormal wall shear stress (WSS). Subsequently, vascular inflammation can trigger a series of biochemical reactions resulting in vascular smooth muscle cell (VSMC) apoptosis and migration, accompanied by inflammatory cell infiltration, secretion of various cytokines, and inflammatory factors. These changes result in degradation of vascular wall, leading to the progression and eventual rupture of IAs. Increasing our knowledge of the pathogenesis of these lesions will offer physicians new options for prevention and treatment. In this study, we review aneurysmal pathogenesis to seek for safe, effective, and non-invasive therapeutic strategies.
Highlights
Saccular intracranial aneurysms (IAs) are the most common cause of subarachnoid hemorrhage (SAH), which resulted in a high mortality and morbidity (Lawton and Vates, 2017)
Under abnormal wall shear stress (WSS), nuclear factor-κB (NF-κB) in cerebral arterial walls upregulates expression of downstream genes, such as monocyte chemoattractant protein 1 (MCP-1) and vascular cell adhesion molecule 1 (VCAM-1) gene, which lead to macrophage infiltration and endothelial dysfunction
Animal models and clinical studies have shown that vascular remodeling and inflammatory cascades were the important mechanism for IA formation, progression, and rupture
Summary
Saccular intracranial aneurysms (IAs) are the most common cause of subarachnoid hemorrhage (SAH), which resulted in a high mortality and morbidity (Lawton and Vates, 2017). Understanding the mechanisms underlying formation, progression, and rupture of IAs may help us to look for potential therapeutic strategy, especially safe and effective non-invasive therapies. Inflammatory cell infiltration, Therapeutic Strategies for Targeting Aneurysm Pathogenesis vascular smooth muscle cells (VSMCs) apoptosis and migration (Figure 1), and extracellular matrix (ECM) protein degradation promoted the progression and rupture of IAs (Hashimoto et al, 2006; Chalouhi et al, 2012; Signorelli et al, 2018). We try to take aim at profiling the pathogenesis mechanism in formation and progression of IAs on the facet of cytology, which has positive impacts on deconstructing and deducing the potential therapeutic targets of IAs (Table 1)
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