**Acknowledgements**

hormonal changes driving aging (endocrine senescence induction) playing a critical role in the

CVD seem to begin as a consequence of a damaging process and endothelial dysfunction, and there are pieces of evidence implying cellular senescence in the functional imbalance of the endothelium. Cellular senescence is a physiological mechanism which occurs as a consequence of aging, but

**Figure 3.** Different characteristics of young and senescent endothelial cells. Senescent cells undergo distinctive phenotypic, morphological alterations and senescence-associated secretory phenotype (SASP). The number of endothelial microvesicles (EMVs) of the senescent cells is greater than those derived from young cells. Also, the reactive oxygen species (ROS) production is higher in senescent endothelial cells compared with young endothelial cells. Moreover, the secretion of growth factors (GF) and proinflammatory cytokines (infl. cytokines) from senescent endothelial cells are reduced.

aging process and adding a new perspective on the mechanisms involved in aging.

**6. Conclusions and perspectives**

62 Endothelial Dysfunction - Old Concepts and New Challenges

This work was supported by Plan Nacional Proyectos de Investigación en Salud of Instituto de Salud Carlos III (ISCIII) Fondos Feder European Grants (PI14/00806 and PI17/01029); Red de Investigación Renal (REDinREN; RD16/0009/0034) Junta de Andalucía Grants, P12-CTS-7352 and Santander Universidad Complutense de Madrid PR41/17-20964. Matilde Alique is a fellow of the program "Ayuda Postdoctoral Programa Propio" from Universidad de Alcalá, Madrid, Spain. Rafael Ramírez-Carracedo is a fellow of the program FPI (Formación de Personal Universitario) from Universidad Francisco de Vitoria, Madrid, Spain".
