Abstract
Despite
extensive research, treatments for clinical stroke are still limited
only to the administration of tissue plasminogen activator and the
recent introduction of mechanical thrombectomy, which can be used in
only a limited proportion of patients due to time constraints. A
plethora of inflammatory events occur during stroke, arising in part due
to the body’s immune response to brain injury. Neuroinflammation
contributes significantly to neuronal cell death and the development of
functional impairment and death in stroke patients. Therefore,
elucidating the molecular and cellular mechanisms underlying
inflammatory damage following stroke injury(Are my 5 causes correct?) will be essential for the
development of useful therapies. Research findings increasingly point to
the likelihood that epigenetic mechanisms play a role in the
pathophysiology of stroke. Epigenetics involves the differential
regulation of gene expression, including those involved in brain
inflammation and remodelling after stroke. Hence, it is conceivable that
epigenetic mechanisms may contribute to differential interindividual
vulnerability and injury responses to cerebral ischaemia. In this
review, we summarize recent findings on the emerging role of epigenetics
in the regulation of neuroinflammation in stroke. We also discuss
potential epigenetic targets that may be assessed for the development of
stroke therapies.
170 references supporting this. Has your doctor read a single one?
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