A different modulation of vascular endothelial growth factor (VEGF) activation in response to hypoxia could cause different clinical pictures in inner ear disorders

Abstract

Abstract When envisaging inner ear damage, the general tendency is to classify the damage into separate entities, according to the differences in clinical presentation, regardless of the frequent absence of a completely satisfactory explanation for the damage and, consequently, absence of a specific therapy. Nevertheless, a common ground can be found in haemodynamic changes and subsequent abnormal vasomotor reaction, which can be responsible for various kinds of labyrinthine effects depending on the extent, the duration and the severity of the consequent ischaemia. A key to a better understanding of the different effects of the resulting ischaemia and hypoxia could be found by considering the regulation of vascular endothelial growth factor (VEGF), which is known as a protective factor for inner ear structures under threat. If the haemodynamic change is mild, the possibility of VEGF up-regulation, which despite its finality could be a trigger for an imbalance of labyrinthine hair cells or fluids, could be a reliable indicator of damage. In contrast, if the vasoconstriction leads to a more severe hypoxia, this could directly lead to an acute, more or less transient damage according to a more direct mechanism. This damage could not, or could only partially, permit a useful activation of VEGF, and the total or partial recovery could therefore depend on the entity of the damage itself and on the efficacy of other, less specific protective endogenous or exogenous factors.