Editorial P 21 Waf 1 / Cip 1 in endothelial cell survival Fawzi Aoudjit

The role of endothelial cells in pathological processes is the focus of intensive research. In this context, programmed cell death (apoptosis) plays an important function. Although apoptosis can be seen in many instances as detrimental in the cardiovascular system, it also has beneficial functions. For example, the occurrence of endothelial cell apoptosis has deleterious effects on the development of the cardiovascular system that lead to embryonal lethality. An increase of apoptosis in endothelial cells also contributes to various pathological conditions such as atherosclerosis, tissue destruction during vascular injury, inflammation and allograft arteriopathy, and cellular resistance to apoptosis is necessary for the maintenance of blood vessel integrity and for angiogenesis [1]. However, in the adult, endothelial cell apoptosis is required to prevent neovascularization [2]. Therefore, the tight regulation of endothelial cell apoptosis and function is of prime importance. The homeostasis and function of endothelial cells are controlled by several chemical signals such as VEGF, vitronectin, nucleotides, oxidized LDL, and their membrane receptors [2]. In addition, growing evidence indicates that mechanical signals are also important in endothelial cell functions as they influence cell shape and structure, growth, and other characteristics. The mechanical signals to which cells are exposed in vivo include gravitational force, mechanical stress and shear stress. Endothelial cells are particularly exposed to the latter force associated with blood flow. They adapt to sustained shear stress, which is believed to shape the vascular bed through remodelling in order to maintain optimal circulation [3]. Mechanical signals generated by shear stress are mediated by several