Cellular senescence, cardiovascular risk, and CKD: a review of established and hypothetical interconnections

Cellular senescence is associated with shortened or damaged telomeres and is characterized by permanent exit from the cell cycle, morphological changes, and altered function. It develops after repeated cell divisions and also can be induced prematurely by stress conditions. The senescent phenotype, depending on cell type and atherosclerosis phase, seems to be a proatherosclerotic one: it promotes endothelial dysfunction and appears to be implicated in plaque destabilization, as well as in endothelial progenitor cell alteration. Many traditional and nontraditional cardiovascular disease risk factors induce senescence in a variety of vascular cells. Several of these factors, such as diabetes, hypertension, oxidative stress, and inflammation, are clustered in patients with chronic kidney disease. In a limited number of recent studies, stress-induced premature cellular senescence in this biologically aged population also was described. The hypothesis that premature cellular senescence might be considered an additional atherosclerosis-inducing factor in patients with chronic kidney disease is proposed.