Leptomeningeal anastomoses: Mechanisms of pial collateral remodeling in ischemic stroke.
Leptomeningeal anastomoses: Mechanisms of pial collateral remodeling in ischemic stroke.
复制标题
软脑膜硬化：缺血性卒中软脑膜侧支重塑的机制。
DOI：
10.1002/wsbm.1553
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发表时间：
2022-07
影响因子：
3.1
通讯作者：
中科院分区：
文献类型：
--
作者：
动脉侧支是由脑膜侧支血管或脑脊膜侧支血管吻合所决定的，在缺血性脑卒中后脑血流恢复和神经系统恢复中发挥着重要作用。除威利斯圈外，脑侧支循环的次级网络作为连接脑膜远端动脉的小动脉发育的残余物存在。最近的兴趣在于了解控制这些预先存在的侧支血管的生长和重塑或动脉形成的细胞和分子适应。动物模型和人类缺血性中风研究的新发现表明，内皮、免疫和血管相关细胞的多因素、复杂的时空相互作用可能共同促进或阻碍动脉发生。这些有价值的报告可能为大血管闭塞患者的枢轴侧支反应的潜在预测因素提供重要的见解，并可能有助于提高侧枝功能和改善卒中恢复的治疗方法。神经系统疾病分子和细胞生理学本文分类如下：LMA生态位内的多种影响汇聚在一起调节动脉发生。
Arterial collateralization, as determined by leptomeningeal anastomoses or pial collateral vessels, is a well‐established vital player in cerebral blood flow restoration and neurological recovery from ischemic stroke. A secondary network of cerebral collateral circulation apart from the Circle of Willis, exist as remnants of arteriole development that connect the distal arteries in the pia mater. Recent interest lies in understanding the cellular and molecular adaptations that control the growth and remodeling, or arteriogenesis, of these pre‐existing collateral vessels. New findings from both animal models and human studies of ischemic stroke suggest a multi‐factorial and complex, temporospatial interplay of endothelium, immune and vessel‐associated cell interactions may work in concert to facilitate or thwart arteriogenesis. These valuable reports may provide critical insight into potential predictors of the pial collateral response in patients with large vessel occlusion and may aid in therapeutics to enhance collateral function and improve recovery from stroke. Neurological Diseases > Molecular and Cellular Physiology This article is categorized under: Multiple levels of influence converge to regulate arteriogenesis within the LMA niche.
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