Daidone Mario, Cataldi Marco, Pinto Antonio, Tuttolomondo Antonino
Department of Health Promotion, Maternal and Infant Care, Internal Medicine and Medical Specialties, "G. D'Alessandro", University of Palermo, Piazza delle Cliniche n.2, Palermo, Italy.
Neural Regen Res. 2021 Nov;16(11):2154-2158. doi: 10.4103/1673-5374.310607.
Ischemic stroke occurs under a variety of clinical conditions and has different pathogeneses, resulting in necrosis of brain parenchyma. Stroke pathogenesis is characterized by neuroinflammation and endothelial dysfunction. Some of the main processes triggered in the early stages of ischemic damage are the rapid activation of resident inflammatory cells (microglia, astrocytes and endothelial cells), inflammatory cytokines, and translocation of intercellular nuclear factors. Inflammation in stroke includes all the processes mentioned above, and it consists of either protective or detrimental effects concerning the "polarization" of these processes. This polarization comes out from the interaction of all the molecular pathways that regulate genome expression: the epigenetic factors. In recent years, new regulation mechanisms have been cleared, and these include non-coding RNAs, adenosine receptors, and the activity of mesenchymal stem/stromal cells and microglia. We reviewed how long non-coding RNA and microRNA have emerged as an essential mediator of some neurological diseases. We also clarified that their roles in cerebral ischemic injury may provide novel targets for the treatment of ischemic stroke. To date, we do not have adequate tools to control pathophysiological processes associated with stroke. Our goal is to review the role of non-coding RNAs and innate immune cells (such as microglia and mesenchymal stem/stromal cells) and the possible therapeutic effects of their modulation in patients with acute ischemic stroke. A better understanding of the mechanisms that influence the "polarization" of the inflammatory response after the acute event seems to be the way to change the natural history of the disease.
缺血性中风在多种临床情况下发生，且具有不同的发病机制，导致脑实质坏死。中风的发病机制以神经炎症和内皮功能障碍为特征。缺血性损伤早期触发的一些主要过程是常驻炎症细胞（小胶质细胞、星形胶质细胞和内皮细胞）的快速激活、炎性细胞因子以及细胞间核因子的易位。中风中的炎症包括上述所有过程，并且就这些过程的“极化”而言，它具有保护或有害作用。这种极化源于调节基因组表达的所有分子途径的相互作用：表观遗传因素。近年来，新的调节机制已被阐明，这些机制包括非编码RNA、腺苷受体以及间充质干/基质细胞和小胶质细胞的活性。我们综述了长链非编码RNA和微小RNA如何成为一些神经疾病的重要介质。我们还阐明了它们在脑缺血损伤中的作用可能为缺血性中风的治疗提供新的靶点。迄今为止，我们尚无足够的工具来控制与中风相关的病理生理过程。我们的目标是综述非编码RNA和先天免疫细胞（如小胶质细胞和间充质干/基质细胞）的作用以及对急性缺血性中风患者进行调节的可能治疗效果。更好地理解急性事件后影响炎症反应“极化”的机制似乎是改变疾病自然病程的途径。
