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This review summarizes the recent advances in molecular mechanisms by which five classes of receptor tyrosine kinases (RTKs) contribute to vascular remodeling.Recent findings have expanded our knowledge regarding RTK regulation. In particular, G-protein-coupled receptors, mineralocorticoid receptors, mechanical and oxidative stresses transactivate RTKs. These receptors are highly interactive with many downstream targets (including tyrosine kinases and other RTKs) and function as key regulatory nodes in a dynamic signaling network. Interactions between vascular and nonvascular (immune and neuronal) cells are controlled by RTKs in vascular remodeling. Inhibition of RTKs could be an advantageous therapeutic strategy for vascular disorders.RTK-dependent signaling is important for regulation of key functions during vascular remodeling. However, current challenges are related to integration of the data on multiple RTKs in vascular pathology.