The etiological origins of ischemic stroke and resulting pathological processes are mediated by a multifaceted cascade of molecular mechanisms that are in part modulated by posttranscriptional activity. Accumulating evidence has revealed a role for microRNAs (miRNAs) as essential mediators of posttranscriptional gene silencing in both the physiology of brain development and pathology of ischemic stroke.
In a review, Li et al. compile miRNAs that have been reported to regulate various stroke risk factors and pre-disease mechanisms, including hypertension, atherosclerosis, and diabetes, followed by an in-depth analysis of miRNAs in ischemic stroke pathogenesis, such as excitotoxicity, oxidative stress, inflammation, apoptosis, angiogenesis and neurogenesis. Since promoting or suppressing expression of miRNAs by specific pharmaceutical and non-pharmaceutical therapies may be beneficial to post-stroke recovery, they also highlight the potential therapeutic value of miRNAs in clinical settings 1).
Atrial fibrillation (AF) is increasingly recognized as the single most important cause of disabling ischemic stroke in the elderly.
Not less than 50% of all ischemic strokes appear to occur resulting from pathology of extracranial arteries. Occlusions and stenoses are more commonly encountered in carotid arteries, with the incidence of occlusion of the internal carotid artery (ICA) ranging from 5 to 10% within the structure of all lesions of brachiocephalic artery (BCA).
Secondary ischemic injury is common after acute brain injury and can be evaluated with the use of neuromonitoring devices.
In brain tissue, a biochemical cascade known as the ischemic cascade is triggered when the tissue becomes ischemic, potentially resulting in damage to and death of brain cells.
Ischemic stroke is a major cause of death and long-term disability worldwide.
Ischemic Stroke (Emergency Management in Neurology) By Giuseppe D'Aliberti, Marco Longoni, Valentina Oppo, Valentina Perini, Luca Valvassori, Simone Vidale, Cristina Motto