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• W82458960 abstract "Hypoxia and ischemia are the most important stimuli for angiogenesis. With severe stenoses, the reduced oxygen and metabolite supply is recognized in the affected muscle tissue by an intracellular sensoring system triggering diverse biological emergency steps. Energy shortage leads to a breakdown of the high energy phosphates, increased concentrations of lactate as a consequence of anaerobic glycolysis and the activation of hypoxia inducible factors, e.g. hypoxia inducible factor 1-α (HIF-1α). Binding of the transcription factor to consensus sequences on corresponding promoters in turn results in an increased expression of genes like vascular endothelial growth factor-A (VEGF-A). The gene products are released from the hypoxic cell resulting in a concentration gradient highest in the hypoxic tissue. Upon binding of VEGF-A to its receptors expressed on endothelial cells, which do not express VEGF-A in vivo, endothelial cells start to proliferate and migrate in direction of the concentration gradient. Capillary sprouting starts, resulting in a network of capillaries surrounding and invading the ischemic and hypoxic tissue. However, since SMCs are not a target for VEGF-A, VEGF-A cannot be part of the interaction between endothelial cells and SMCs, the main players in arteriogenesis. Only muscular collateral arteries and not capillaries are able to supply enough blood from outside the risk region to prevent the consequences of severe ischemia. Collateral artery growth does not necessarily take place within hypoxic tissue. The arterial tissue itself, constantly bathed in oxygen-rich blood, never gets hypoxic. Since it has never been analyzed whether there exists a causal relation between ischemia and col-" @default.
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• W82458960 date "2006-01-05" @default.
• W82458960 modified "2023-09-24" @default.
• W82458960 title "Role of Hypoxia/lschemia/VEGF-A, and Strain Differences" @default.
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• W82458960 doi "https://doi.org/10.1007/1-4020-8126-x_6" @default.
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