domingo, 5 de febrero de 2017

Inflammation and atherosclerosis

I just read "Fine-tuning inflammation-resolution programs: focus on atherosclerosis" (Fredman, Sadhu and Rymut, 2017). I really liked this article, because it provides more concrete information about the concept of "low grade chronic inflammation" that characterizes chronic diseases,  such as cardiovascular disease, obesity, arthritis or depression.

Fredman et al exemplify the concept through atherosclerosis. In this condition the plaques that appear in blood vessels are similar to "unresolved vascular wounds", in which the inflammatory process occurs. But this inflammation does not resolve the lesion, so the inflamed plaque persists over time, as shown in the figure below.

Basically there is an imbalance between agents that promote inflammation: LT (leukotrienes), PG (prostaglandins); and those who slow it down (SPM: specialized proresolving mediators) (1). 

The figure shown below differentiates an atherosclerotic plaque where this imbalance exists (on the left), and a plaque dominated by the SPM (on the right) -in a mouse model- (1).

The most common outcome is a self-limiting inflammation, as shown in the upper left figure of the figure below: the inflammation begins, reaches a peak and then recedes until it disappears. In chronic inflammation, once the inflammatory peak is reached, it persists over time, as shown in the upper right chart.

The lower graph of the figure presents a therapeutic scheme to stop this disease: to identify mediators and mechanisms associated with inflammation, combined with drugs that influence the same.

The article proposes that the treatment of these diseases can be designed to modulate the immune response causing the damage,  without canceling its beneficial effect completely, through a potentiation of  specialized proresolving mediators (1).


(1) Fredman G, Sadhu S, Rymut N. Fine-tuning inflammation-resolution programs; focus on atherosclerosis. Review. Curr Opin Clin Nutr Metab Metab Care 2017;20(2):117-123.

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