There is an increasing prevalence of Vascular Cognitive Impairment (VCI) worldwide, and several studies have suggested that Chronic Cerebral Hypoperfusion (CCH) plays a critical role in disease onset and progression. However, there is a limited understanding of the underlying pathophysiology of VCI, especially in relation to CCH. Neuroinflammation is a significant contributor in the progression of VCI as increased systemic levels of the proinflammatory cytokine interleukin-1β (IL-1β) has been extensively reported in VCI patients. Recently it has been established that CCH can activate the inflammasome signaling pathways, involving NLRP3 and AIM2 inflammasomes that critically regulate IL-1β production. Given that neuroinflammation is an early event in VCI, it is important that we understand its molecular and cellular mechanisms to enable development of disease-modifying treatments to reduce the structural brain damage and cognitive deficits that are observed clinically in the elderly. Hence, this review aims to provide a comprehensive insight into the molecular and cellular mechanisms involved in the pathogenesis of CCH-induced inflammasome signaling in VCI.

中文翻译：

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炎症小体在血管性认知障碍中的作用

世界范围内血管性认知障碍 (VCI) 的患病率越来越高，一些研究表明，慢性脑低灌注 (CCH) 在疾病发作和进展中起关键作用。然而，对 VCI 的潜在病理生理学了解有限，尤其是与 CCH 相关的情况。神经炎症是 VCI 进展的重要因素，因为已在 VCI 患者中广泛报道促炎细胞因子白细胞介素 1β (IL-1β) 的全身水平升高。最近已经确定 CCH 可以激活炎性体信号通路，包括关键调节 IL-1β 产生的 NLRP3 和 AIM2 炎性体。鉴于神经炎症是 VCI 的早期事件，重要的是，我们了解其分子和细胞机制，以便能够开发改善疾病的治疗方法，以减少在老年人中临床观察到的结构性脑损伤和认知缺陷。因此，本综述旨在全面了解参与 CCH 诱导的 VCI 炎症小体信号传导的发病机制的分子和细胞机制。