Senescence in the Cardiovascular System

Dear Colleagues,

Aging and senescence are related closely. Aging is the major risk factor for cardiovascular diseases and cardiovascular disease is the leading cause of death in the aged population. With the increase in life expectancy worldwide, the impact of cardiovascular diseases increases despite continuous progress in medicine. Senescence has been described more than 50 years ago in fibroblasts in culture and is characterized as irreversible cell cycle arrest independent of quiescence and terminal differentiation. More recent data suggest that cell senescence in a certain context in vivo might not be irreversible. This could provide additional opportunities to modify this cellular response to improve healthy aging. Traditionally, cardiovascular research related to senescence focused on the endothelium. Increasing evidence supports a much more complex interaction between endothelial cells, immune cells, smooth muscle, astrocytes in the blood–brain barrier, and adipocytes in cardiometabolic disorders. Further complexity is added by differences in endothelial function in distinct vascular beds. In general, vascular senescence is considered as detrimental while senescent liver endothelial cells fulfill important metabolic functions and are required for healthy ageing.

An additional important feature of senescence is the senescence-associated secretory phenotype (SASP). Detrimental effects are thought to be due to the release of this cocktail of secreted factors from senescent cells. However, recently established ablator and reporter mouse models suggest that senescent cells, SASP, and functions are different between P16INK4A and P21 expressing cell types questioning the concept of “the” senescent cell and “the SASP”.

All contributions shedding additional light and providing significant or provocative findings in the field of senescence in the cardiovascular system are welcome in this Special Issue of Cells.

Dr. Kay-Dietrich Wagner
Guest Editor

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