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缺血性脑卒中发病机制中的血管内皮功能障碍和炎症。

Endothelial Dysfunction and Inflammation in Ischemic Stroke Pathogenesis.

机构信息

Department of Health Promotion, Maternal and Infant Care, Internal Medicine and Medical Specialties, "G. D'Alessandro", University of Palermo, Piazza delle Cliniche n.2, 90127 Palermo, Italy.

出版信息

Curr Pharm Des. 2020;26(34):4209-4219. doi: 10.2174/1381612826666200417154126.

Abstract

Stroke is a heterogeneous disease, and within the broad category of brain ischemia and its subtypes vary dramatically in its etiology. The endothelium can regulate the vascular homeostasis by modulating processes of vascular dilation and constriction by producing and secreting cytokines and chemical mediators, and inflammation represents one of the most important factors that contribute to alteration in vessel structure and function by dysregulation of this fine balance. Endothelial dysfunction means a basic determinant of the vascular damage, which can be identified in all different clinical subtypes of stroke, and, recently, it has been recognized as an interesting determinant of cerebrovascular risk. The entire spectrum of inflammatory processes is likely to act in concert, and cytokines are important mediators of stroke by inducing immunological/inflammatory reactions, which contribute to brain infarct progression as well as to the disease severity and outcome. Results from recent studies and ongoing and future researches will allow characterizing these complex mechanisms better and finally leading to innovative therapeutic strategies that may change the natural history of this severe and disabling disease significantly.

摘要

中风是一种异质性疾病,在广泛的脑缺血类别及其亚型中,其病因差异很大。内皮细胞通过产生和分泌细胞因子和化学介质来调节血管扩张和收缩过程,从而调节血管内稳态,炎症是通过这种精细平衡的失调导致血管结构和功能改变的最重要因素之一。内皮功能障碍是血管损伤的基本决定因素,可在中风的所有不同临床亚型中识别出来,最近,它已被认为是脑血管风险的一个有趣决定因素。整个炎症过程谱可能协同作用,细胞因子通过诱导免疫/炎症反应在中风中起重要作用,这些反应有助于脑梗死进展以及疾病严重程度和结局。最近的研究结果以及正在进行和未来的研究将使我们能够更好地描述这些复杂的机制,并最终导致创新的治疗策略,这些策略可能会显著改变这种严重和致残疾病的自然病程。

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