Hypertension, high blood pressure, is caused by arterial stiffness, which is in turn caused by a combination of mechanisms such as the accumulation of persistent cross-links that alter the structural properties of tissue, and chronic inflammation produced by senescent cells that alters the behavior of cells in blood vessel walls. Hypertension damages fragile tissues, causes the muscle of the heart to become larger and weaker, and ultimately interacts with the corrosive effects of atherosclerosis on blood vessel walls to produce a fatal rupture, leading to a stroke or heart attack.
The work noted here is representative of most efforts to safely lower blood pressure, in that it attempts to force cellular mechanisms in blood vessel walls into a more functional state without addressing the underlying causes of dysfunction – those that stiffen blood vessels. All too much of medical research has this focus: tinker with cell state in patients, but don’t repair the damage that is causing those cells to run awry.
In the case of raised blood pressure, however, this condition directly causes a varied package of downstream harm, and is an important mediating mechanism between
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