Non-coding RNAs and other determinants of neuroinflammation and endothelial dysfunction: regulation of gene expression in the acute phase of ischemic stroke and possible therapeutic applications

Ischemic stroke occurs under a variety of clinical conditions and has different pathogeneses, resulting in necrosis brain parenchyma. Stroke pathogenesis is characterized by neuroinflammation endothelial dysfunction. Some the main processes triggered early stages ischemic damage are rapid activation resident inflammatory cells (microglia, astrocytes cells), cytokines, translocation intercellular nuclear factors. Inflammation includes all mentioned above, it consists either protective or detrimental effects concerning “polarization” these processes. This polarization comes out from interaction molecular pathways that regulate genome expression: epigenetic In recent years, new regulation mechanisms have been cleared, include non-coding RNAs, adenosine receptors, activity mesenchymal stem/stromal microglia. We reviewed how long RNA microRNA emerged as an essential mediator some neurological diseases. also clarified their roles cerebral injury may provide novel targets for treatment stroke. To date, we do not adequate tools to control pathophysiological associated with Our goal review role RNAs innate immune (such microglia cells) possible therapeutic modulation patients acute A better understanding influence response after event seems be way change natural history disease.