Chronic Inflammation Chews Up Your Blood Vessels

A number of the most serious age-related conditions involve the progressive structural and functional decay of your blood vessels. A number of different forms of cellular and molecular damage conspire to clog, weaken, and stiffen blood vessels until one of these small but vital pieces of the body's infrastructure fails catastrophically, and then a blockage or a bleed causes death or crippling injury in a matter of moments. The older you are the more extensive the damage and the worse the odds, but poor lifestyle choices will generally put you in a poorer position than would otherwise be the case.

Chronic inflammation is a noteworthy contribution to many issues associated with aging, and it is one of the contributing causes that most of us have a fair level of control over throughout most of our lives. By taking basic good care of health matters, exercising, and eating a diet low enough in calories to stay slim, the average individual will have a lower level of inflammation as a result. Inflammation is probably a primary mechanism in the link between excess fat tissue and raised risk of suffering from all of the common age-related disease. Visceral fat tissue is metabolically active in ways that promote inflammation, and the more of it you have the worse off you are. You can't escape chronic inflammation in aging entirely by staying thin and active, however, as significant raised inflammation levels also result from the characteristic age-related failure of the immune system. As a result of the damage of aging, the immune system becomes both ineffective and constantly overactive at the same time.

Why exactly is chronic inflammation bad? What does it do under the hood? There are many distinct mechanisms, but here are some papers to illustrate a couple that involve your blood vessels. In effect you might think of inflammatory processes as gnawing away at the structural integrity of these important tissues, at an insignificant pace in youth, but accelerating over the years. There is always repair taking place as well, of course, but ultimately the inflammation wins - or at least that will be the case until the research community is given enough support and funding to produce the means to reverse these mechanisms.

A Crucial Role for CDC42 in Senescence-Associated Inflammation and Atherosclerosis

Chronic inflammation is characterized by the long-term presence of immune cells in affected tissues and is associated with age-related diseases such as cancer, neurodegenerative disorders, and cardiovascular disease. Interestingly, levels of pro-inflammatory cytokines are elevated in the endothelial cells and serum of older persons in the absence of disease. Thus, inflammation that accompanies the natural aging process may contribute to the onset of age-related diseases, which are responsible for most of the mortality in modern societies.

Atherosclerosis is an age-related chronic inflammatory disease. In persons with atherosclerosis, chronic inflammation is mainly induced by sterile stimuli and it accelerates disease progression. The initial step of the atherosclerotic process involves recruitment of inflammatory monocytes to dysfunctional endothelial cells. Senescent endothelial cells have been suggested to represent "dysfunctional endothelial cells" since they are specifically localized in the atherosclerotic lesions of patients and share many common features, including the pro-inflammatory phenotype that can induce sterile inflammation related to atherosclerosis. Although senescence of endothelial cells has been implicated in the process of atherogenesis, a specific role of senescent endothelial cells in chronic inflammation associated with atherosclerosis remains uncertain due to the lack of in vivo models. The molecular mechanisms underlying the pro-inflammatory phenotype in senescent endothelial cells also remain unclear [but we] identified CDC42 signaling as a mediator of chronic inflammation associated with endothelial senescence.

Mesenchymal stem cells for treatment of aortic aneurysms

An aortic aneurysm (AA) is a silent but life-threatening disease that involves rupture. It occurs mainly in aging and severe atherosclerotic damage of the aortic wall. Even though surgical intervention is effective to prevent rupture, surgery for the thoracic and thoraco-abdominal aorta is an invasive procedure with high mortality. Therefore, an alternative strategy for treatment of AA is required. Recently, the molecular pathology of AA has been clarified. AA is caused by an imbalance between the synthesis and degradation of extracellular matrices in the aortic wall. Chronic inflammation enhances the degradation of matrices directly and indirectly, making control of the chronic inflammation crucial for aneurysmal development.

Meanwhile, mesenchymal stem cells (MSCs) are known to be obtained from an adult population and to differentiate into various types of cells. In addition, MSCs have not only the potential anti-inflammatory and immunosuppressive properties but also can be recruited into damaged tissue. MSCs have been widely used as a source for cell therapy to treat various diseases involving graft-versus-host disease, stroke, myocardial infarction, and chronic inflammatory disease such as Crohn's disease clinically. Therefore, administration of MSCs might be available to treat AA using anti-inflammatory and immnosuppressive properties.


This research presents even more reasons to be excited about the Mayo clinic's work on senescent cell clearance and that Spanish group's work on gated mesoporous nanoparticles to destroy senescent cells. Hopefully we will hear more from them soon! I am especially looking forward to future publications from the Spanish group, as their work seems directly applicable as a near-term treatment for what is emerging as one of the significant sources of the damage that constitutes aging.

Posted by: gheme at August 12th, 2014 7:50 AM

I am 94 in good health. I play 9 holes of golf six days a week. For over ten years I was taking 9 grams of fish oil a day. Each gram had 200 mg of DHA. I now take six grams a day. I take alpa lipoic acid. I take 10,000 units of D-3 every day. What else should I take?

Posted by: william kirk at September 4th, 2014 12:35 PM

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