A few different mechanisms plausibly contribute to the stiffening of blood vessels that takes place with aging. This is one of the most harmful aspects of aging, as it causes hypertension by upsetting the feedback mechanisms that control blood pressure. Hypertension in turn damages organ tissues, weakens the heart, and raises the risk of fatal rupture of a weakened blood vessel. The mechanisms of interest include (a) calcification, which may be secondary to inflammation and cellular senescence, (b) the formation of persistent cross-links in the extracellular matrix, degrading structural properties such as elasticity, and (c) dysfunction in the smooth muscle responsible for contraction and dilation of blood vessels.

We can hope that calcification will be improved by senolytic therapies to clear senescent cells, and that near future cross-link breakers based on programs funded by the SENS Research Foundation will make short work of that contribution of cross-links to degenerative aging. Dysfunctional smooth muscle cells are more of a problem, however, as it is far from clear as to what exactly is going wrong and how it might be effectively addressed. In this paper, the researchers mount what I think is a fairly convincing demonstration that this cellular dysfunction is significant and distinct from other factors related to vascular stiffening, and is inherent to the cells rather than being caused directly by the environment of the surrounding aged tissue. This calls for more attention to be directed towards this part of the problem.

Link: https://doi.org/10.1111/acel.12748