Av Søren Beck Jensen
Postdoktor ved TREC
Endothelial cells line the interior surface of the blood vessels. Microparticles first described as cellular dust, are shed by endothelial cells to convey information via the blood stream. Recent research published in “Circulation” suggests that blood-borne microparticles from patients with acute coronary syndrome conveys a message that leads to premature aging of the endothelium, which may result in future cardiovascular disease.
The study investigates the biological signal from blood-borne microparticles and how it promotes untimely cellular aging. By applying drugs in cell cultures the study outlines some of the mechanisms that propagates the microparticle caused premature aging of endothelial cells. A small protein named Angiotensin II bears a key responsibility in conveying the deleterious signal. The study shows how prematurely aged endothelial cells lose their ability to prevent platelets aggregation, an indication of the adverse consequence of endothelium aging: Increased risk of cardiovascular disease.
The researchers conclude that during acute coronary syndrome it may be of value to target the production of microparticles or the signaling they convey that results in premature endothelium aging. The study suggests blockade of the Angiotensin II signal as a potential drug target that could kill the messenger who brings the unpleasant message.
Translational science aims to make basic research laboratory findings useful and relevant to clinical research and practice. The bridge between basic science and clinical applicability is often long and rarely straight. For the study summarized here, I believe further studies are required to fully outline the clinical potential for findings. Until then: Please do not kill the messenger.
Reference: Abbas M, Jesel L, Auger C, Amoura L, Messas N, Manin G, et al. Endothelial Microparticles From Acute Coronary Syndrome Patients Induce Premature Coronary Artery Endothelial Cell Aging and Thrombogenicity: Role of the Ang II/AT1 Receptor/NADPH Oxidase-Mediated Activation of MAPKs and PI3-Kinase Pathways. Circulation (2017).