Do Smooth Muscle Cells Contribute to Arterial Stiffening?
Vascular stiffening is a major cause of cardiovascular aging. It alone is enough to explain the age-related onset of hypertension, for example, which in turn deforms blood vessels and the heart, and causes ongoing harm to the brain where small blood vessels fail under stress, among other issues. Much of the cause of loss of elasticity in blood vessels is thought to be caused by cross-linking and calcification in the extracellular matrix, processes that occur as a side-effect of the normal operation of metabolism, and which could be reversed with suitably designed drugs. Unfortunately there is still comparatively little research focused on these targets, certainly nowhere near as much as is merited by the consequences of these contributing causes of degenerative aging.
Here, researchers identify another potential causative agent in the stiffening of blood vessels, in changing behaviors and characteristics of the smooth muscle cells that surround blood vessels. Is this a primary cause or a reaction to primary causes, however? More research is needed on that topic, as is often the case:
Arterial and vascular stiffness occurs through the normal process of biological aging and is associated with an increased risk of heart attacks and strokes. As we age, the aorta, which normally acts as a shock absorber dampening the pulse associated with each heartbeat, tightens and becomes rigid, causing a host of problems including high blood pressure, increased risk of adverse cardiovascular events and even death. In the United States, the risk of developing hypertension due to aging is greater than 90 percent in both men and women. Recent studies have identified several mechanisms for arterial stiffness in humans. Research has focused on the structural matrix proteins, or non-living components that compose the outer walls of blood vessels, as well as endothelial cells which line the inner portion of the vascular walls.Researchers have focused on a new potential source - smooth muscle cells that are a major component of the "middle" of the blood vessel wall. The team isolated aortic cells from normal and hypertensive rat models in both young and aged animals. Then, using atomic force microscopy, an advanced microscope that incorporates a tiny probe that can interact with single cells and molecules, the team measured the compression force of the needle against the specimen and how the tip adhered to or "stuck" to smooth muscle cells.
"We found that hypertension increased both vascular smooth cell stiffness and adhesion or stickiness, and that these changes were augmented by aging. Our results are adding to our understanding and taking studies in a different direction. Although all cells are contributing to arterial stiffness, it's important to identify the order in which they're adding to the problem. Identifying smooth muscle cells as a contributor can help identify possible preventatives and potential drugs to counteract and reverse the disease and keep vessels healthier as we age."
Does anybody have a study made in the USA, that conclude that people thought that an increase in human lifespan was not a good idea, and they would like to die around 100, more or less?
Hello Josep, have you seen this videos ? Maybe I can't call this video a study, but it worth seeing.
Eternal Life Conversations - Episode 1 - 6
https://www.youtube.com/user/EternalLifeFan
@Josep: You might be thinking of the Pew study from 2013?
https://www.fightaging.org/archives/2013/08/people-want-the-better-end-of-what-exists-but-more-than-that-isnt-within-their-horizons.php
Reason, is there anything people can currently do to prevent or reduce the problem of arterial stiffening and calcification?
@JC: From a practical point of view, nothing more than the slight slowing of the process you get from exercise and calorie restriction. I'm not aware of anything shown to do better that is something you can easily get hold of or make use of.
As for so many of these things, the realistic hope is to redirect some early stage research into SENS-like directions such that existing research groups pick up on early demonstrations of effectiveness in the lab and put in more of the legwork to generate viable treatments.
Senlyotics could well arrive soon. SENS is working on this too and is making good progress last I heard. There is interest in this area of research from various quarters so I think this will yield results sooner rather than later.
Gene therapy such as Miyo-Statin inhibition possibly has plaque ablation side effects which could also be used in a SENS approach. Follistatin in particular has been used to treat Beckers MD and shown promising results and a side effect may be reduction of plaque. Miyostatin in hibition has been shown to reduce plaque in mice for example:
http://www.ncbi.nlm.nih.gov/pubmed/19509018
Again this could be used as a SENS approach should the foam cell removal SENSRF are working on not be ready in time for a first pass. The caveat is in the study it was a mutant mouse strain but there are reports from elsewhere that Mstn in hibition can mitigate plaques.
Arterial stiffening could be addressed by rejuvenating Telomeres as Dr Fossel eludes to, the heart does not fail us the tissues connected to it do and they can be and have been shown to be rejuvenated using TERT. This is not a popular approach with SENS but personally I think telomerase is a powerful rejuvenator that should be tested in people. Dr Fossel believes so and his project Telocyte plans to bring Telomerase therapy to people via the FDA soon.
There are a number of promising therapies around and no one school of thought is likely to have all the answers but there are things we can support now to get them tested soon.