Stroke is a heterogeneous disease, and within the broad category of brain ischemia and its subtypes
vary dramatically in its etiology.
The endothelium can regulate the vascular homeostasis by modulating processes of vascular dilation and constriction
by producing and secreting cytokines and chemical mediators, and inflammation represents one of the most
important factors that contribute to alteration in vessel structure and function by dysregulation of this fine balance.
Endothelial dysfunction means a basic determinant of the vascular damage, which can be identified in all different
clinical subtypes of stroke, and, recently, it has been recognized as an interesting determinant of cerebrovascular
risk. The entire spectrum of inflammatory processes is likely to act in concert, and cytokines are important
mediators of stroke by inducing immunological/inflammatory reactions, which contribute to brain infarct progression
as well as to the disease severity and outcome.
Results from recent studies and ongoing and future researches will allow characterizing these complex mechanisms
better and finally leading to innovative therapeutic strategies that may change the natural history of this
severe and disabling disease significantly.