Ramírez, RafaelCeprián Costoso, NoemíFiguer, AndreaValera Arévalo, GemmaBodega, GuillermoAlique, MatildeCarracedo Añón, Julia María2023-06-222023-06-222022-02-04Electronic: 2075-442610.3390/jpm12020215https://hdl.handle.net/20.500.14352/71673Atherosclerosis is probably one of the paradigms of disease linked to aging. Underlying the physiopathology of atherosclerosis are cellular senescence, oxidative stress, and inflammation. These factors are increased in the elderly and from chronic disease patients. Elevated levels of oxidative stress affect cellular function and metabolism, inducing senescence. This senescence modifies the cell phenotype into a senescent secretory phenotype. This phenotype activates immune cells, leading to chronic systemic inflammation. Moreover, due to their secretory phenotype, senescence cells present an increased release of highlighted extracellular vesicles that will change nearby/neighborhood cells and paracrine signaling. For this reason, searching for specific senescent cell biomarkers and therapies against the development/killing of senescent cells has become relevant. Recently, senomorphic and senolityc drugs have become relevant in slowing down or eliminating senescence cells. However, even though they have shown promising results in experimental studies, their clinical use is still yet to be determined.engAtribución 3.0 Españahttps://creativecommons.org/licenses/by/3.0/es/journal articlehttps://doi.org/10.3390/jpm12020215https://www.mdpi.com/2075-4426/12/2/215open access612.67616.13AtherosclerosisCellular senescenceEndothelial senescenceExtracellular vesiclesInflammationSenolitycFisiologíaSistema cardiovascular2411 Fisiología Humana2411.03 Fisiología Cardiovascular