Abstract
Among the causes of global death and disability, ischemic stroke (also known as cerebral ischemia) plays a pivotal role, by determining the highest number of worldwide mortality, behind cardiomyopathies, affecting 30 million people. The etiopathogenetic burden of a cerebrovascular accident could be brain ischemia (~80%) or intracranial hemorrhage (~20%). The most common site when ischemia occurs is the one is perfused by middle cerebral arteries. Worse prognosis and disablement consequent to brain damage occur in elderly patients or affected by neurological impairment, hypertension, dyslipidemia, and diabetes. Since, in the coming years, estimates predict an exponential increase of people who have diabetes, the disease mentioned above constitutes together with stroke a severe social and economic burden. In diabetic patients after an ischemic stroke, an exorbitant activation of inflammatory molecular pathways and ongoing inflammation is responsible for more severe brain injury and impairment, promoting the advancement of ischemic stroke and diabetes. Considering that the ominous prognosis of ischemic brain damage could by partially clarified by way of already known risk factors the auspice would be modifying poor outcome in the post-stroke phase detecting novel biomolecules associated with poor prognosis and targeting them for revolutionary therapeutic strategies.
Highlights
Other molecules such as NLRP3 inflammasome, DKK-3, Dectin-1, MKEY, and microRNAs are implicated in neuroinflammation so ongoing, and future researches about the intricate mechanism related could lead to pioneering therapeutic interventions that could considerably modify the natural course of this invalidating condition
The loss of interplay between CD200-CD200R will induce microglial proliferation and activation that may exacerbate the process of neuroinflammation and aggravate the prognosis after stroke
One of these inflammatory pathways, which plays a pivotal role in neuroinflammation, is mediated by Dectin-1 and Syk, a protein with tyrosine kinase activity mainly expressed in microglia
Summary
Stroke is termed as a sudden onset of focal or global symptoms and clinical signs, due to an abrupt occlusion or rupture of a blood cerebral vessel which determines consequential brain suffering through cerebral hypoperfusion or resultant compression by hemorrhage. The onset of neuroinflammation after brain injury is mediated by mediators like “TNF-α, IL1α, IL1β, CXCL7, CCL5, CXCL4, CX3CL1, adhesion molecules, proteases, prostanoids, and leukotrienes”; “IL-1, IL-10, TNF-α, IL- 6, IL-20, IL-17”, and “NADPH oxidase, CXCL8, iNOS, and COX-2” are involved in the phase of boosting of this process and other molecules including “TGF-β, IL-17, IL-10, and IL-23” mediate its termination [5] Other molecules such as NLRP3 inflammasome, DKK-3, Dectin-1, MKEY, and microRNAs are implicated in neuroinflammation so ongoing, and future researches about the intricate mechanism related could lead to pioneering therapeutic interventions that could considerably modify the natural course of this invalidating condition. We have chosen to deepen some biomolecules and related pathways which are described in very recent researches in literature and whose modulation probably could circumscribe the damaged area after a stroke, preventing the ruinous effects of inflammation on brain lesion
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