Cellular senescence denote cells that have entered a status of arrested growth in reaction to cellular damage (Figure ). Thus, senescent cells lose productiveness and no longer divide; they also trigger growth in inflammation, which can aggravate aging. Even though all cell types are able to undergo senescence upon aging, it mainly impact fibroblasts, endothelial cells, and immune cells. Even post-mitotic or slowly proliferating cells, such as the brain or the heart cells, may experience senescence. Senescent cells exhibit modifications in their metabolic activity, undergo significant changes in gene expression, and develop a complex senescence-associated secretory phenotype (SASP), composed of proinflammatory cytokines, chemokines, growth factors, and matrix-remodeling enzymes able to alter their microenvironment. Cellular senescence can impair tissue repair and regeneration, thereby promoting aging. Cellular senescence has been associated with multiple ageinitiated disorders, such as cancer, diabetes, osteoporosis, cardiovascular disorders, stroke, Alzheimer's disease and dementias, as well as osteoarthritis. It has also been related to declines in eyesight, mobility, and cognitive capability.