Senescent Cell Extracellular Vesicles in Vascular Calcification
A growing body of evidence implicates the presence of senescent cells in the development of vascular calcification. Calcification arises as cells in blood vessel walls inappropriately take on the characteristics of bone cells. Senescent cells produce inflammatory signaling that contributes to these and other detrimental changes, and much of that signaling is carried in extracellular vesicles, membrane-wrapped packages of molecules that pass between cells in tissue. The direct solution to this problem is targeted removal of senescent cells, via senolytic therapies, but that isn't stopping researchers from mapping the way in which senescent cell signaling causes dysfunction.
Vascular calcification is an irreversible pathological process associated with a loss of vascular wall function. This process occurs as a result of aging and age-related diseases, such as cardiovascular and chronic kidney diseases, and leads to comorbidities. During these age-related diseases, the endothelium accumulates senescent cells, which stimulate calcification in vascular smooth muscle cells. Currently, vascular calcification is a silent pathology, and there are no early diagnostic tools. Therefore, by the time vascular calcification is diagnosed, it is usually untreatable.
Some mediators, such as oxidative stress, inflammation, and extracellular vesicles, are inducers and promoters of vascular calcification. They play a crucial role during vascular generation and the progression of vascular calcification. Extracellular vesicles, mainly derived from injured endothelial cells that have acquired a senescent phenotype, contribute to calcification in a manner mostly dependent on two factors: (1) the number of extracellular vesicles released, and (2) their cargo. In this review, we present state-of-the-art knowledge on the composition and functions of extracellular vesicles involved in the generation and progression of vascular calcification.
I suspect that as usual in biology it is more complicated. Probably there are some pro-calcification signals which are not directly related to senescent cells. So this research might be useful to cover that part too.