PDF(Pubmed)
Abstract：
Acute ischemic stroke (AIS) remains a major cause of mortality and long-term disability worldwide, driven by complex and multifaceted etiological factors. Metabolic dysregulation, gastrointestinal microbiome alterations, and systemic inflammation are emerging as significant contributors to AIS pathogenesis. This review addresses the critical need to understand how these factors interact to influence AIS risk and outcomes. We aim to elucidate the roles of dysregulated adipokines in obesity, the impact of gut microbiota disruptions, and the neuroinflammatory cascade initiated by lipopolysaccharides (LPS) in AIS. Dysregulated adipokines in obesity exacerbate inflammatory responses, increasing AIS risk and severity. Disruptions in the gut microbiota and subsequent LPS-induced neuroinflammation further link systemic inflammation to AIS. Advances in neuroimaging and biomarker development have improved diagnostic precision. Here, we highlight the need for a multifaceted approach to AIS management, integrating metabolic, microbiota, and inflammatory insights. Potential therapeutic strategies targeting these pathways could significantly improve AIS prevention and treatment. Future research should focus on further elucidating these pathways and developing targeted interventions to mitigate the impacts of metabolic dysregulation, microbiome imbalances, and inflammation on AIS.
摘要：
急性缺血性卒中（AIS）仍然是全球范围内死亡和长期残疾的主要原因。由复杂和多方面的病因因素驱动。代谢失调,胃肠道微生物组改变，和全身性炎症正在成为AIS发病机制的重要贡献者。这篇综述解决了了解这些因素如何相互作用以影响AIS风险和结果的迫切需要。我们的目的是阐明失调的脂肪因子在肥胖中的作用，肠道微生物群破坏的影响，和AIS中由脂多糖（LPS）引发的神经炎症级联反应。肥胖中脂肪因子失调加剧炎症反应，增加AIS风险和严重程度。肠道微生物群的破坏和随后的LPS诱导的神经炎症进一步将全身性炎症与AIS联系起来。神经影像学和生物标志物开发的进展提高了诊断精度。这里,我们强调AIS管理需要多方面的方法，整合代谢，微生物群,和煽动性的见解。针对这些途径的潜在治疗策略可以显着改善AIS的预防和治疗。未来的研究应该集中在进一步阐明这些途径，并开发有针对性的干预措施，以减轻代谢失调的影响。微生物组失衡,和AIS上的炎症。
