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- W1567709724 endingPage "149" @default.
- W1567709724 startingPage "107" @default.
- W1567709724 abstract "Research into areas as divergent as hemangiopoiesis and cardiogenesis as well as investigations of diseases such as cancer and diabetic retinopathy have converged to form the face of research in vascular development today. This convergence of disparate topics has resulted in rapid advances in many areas of vascular research. The focus of this review has been the role of cell interactions in the development of the vascular system, but we have included discussions of pathology where the mechanism of disease progression may have parallels with developmental processes. A number of intriguing questions remain unanswered. For example, what triggers abnormal angiogenesis in the disease state? Are the mechanisms similar to those that control developmental neovascularization? Perhaps the difference in development in angiogenesis versus in disease is context driven, that is, an adult versus an embryonic organism. If this is the case, can the controls that curtail developmental vessel formation be applied in pathologies? Can cell interactions be targeted as a control point for new vessel formation? For instance, can perivascular cells be stimulated or eliminated to result in increased vessel stability or instability, respectively? If the hypothesis that mural cell association is required for vessel stabilization is accurate, are there mechanisms to promote or inhibit mural cell recruitment and differentiation as needed? These and other questions lie in wait for the next generation of approaches to discern the mechanisms and the nature of the cell interactions and the influence of the microenvironment on vascular development." @default.
- W1567709724 created "2016-06-24" @default.
- W1567709724 creator A5041333488 @default.
- W1567709724 creator A5061861542 @default.
- W1567709724 date "2001-01-01" @default.
- W1567709724 modified "2023-10-18" @default.
- W1567709724 title "Cell cell interactions in vascular development" @default.
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