18.03.2014 Aufrufe

Jahresbericht der Klinik - Klinik für Kardiologie - UniversitätsSpital ...

Jahresbericht der Klinik - Klinik für Kardiologie - UniversitätsSpital ...

Jahresbericht der Klinik - Klinik für Kardiologie - UniversitätsSpital ...

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Giovanni G. Camici, PhD<br />

Research Coordinator & Group Lea<strong>der</strong><br />

Basic Cardiovascular Research<br />

Vascular Aging, ACS and Stroke<br />

Due to the progressively aging population, aging represents a crucial<br />

research topic and vascular aging is the research focus of the group<br />

headed by Dr. Giovanni G. Camici. Aging is a major risk factor for the<br />

development of cardiovascular diseases, however, its direct effects<br />

on the cardiovascular systems are not clear since it always occurs in<br />

parallel to atherosclerosis and other risk factors.<br />

Mice offer an ideal model to study aging since they do not spontaneously<br />

develop atherosclerosis or age-related risk factors. However,<br />

they still show an age-dependent decay in vascular function [Fig. 2<br />

and 3]. Based on this model, Dr. Simon Stämpfli recently demonstrated<br />

that aging per se – contrary to the common belief – does not<br />

worsen arterial thrombosis, un<strong>der</strong>scoring the importance of controlling<br />

modifiable risk factors.<br />

In this context, several genes implicated in promoting vascular aging<br />

and age-related cardiovascular disease are a major research focus;<br />

amongst these the adaptor protein p66Shc, the MAP Kinase JNK and<br />

PKC beta. Recently, F. C. Franzeck, D. Hof and R. D. Spescha showed<br />

that some of these genes, namely p66Shc, are similarly upregulated<br />

in patients suffering from acute coronary syndromes [Fig. 1] un<strong>der</strong>lining<br />

that aging genes also play a role in cardiovascular disease.<br />

Fig. 2 Giovanni G. Camici (PhD) and Stephan Keller (Chief Technician)<br />

are assessing the morphological alterations of an aged mouse brain<br />

after middle cerebral artery occlusion / reperfusion.<br />

1.5 × 10 −4<br />

p = 0.0249<br />

p = 0.007<br />

ΔCt (p66shc / S18 rRNA)<br />

1.0 × 10 −4<br />

p = 0.367<br />

5.0 × 10 −5 0<br />

Control<br />

CAD<br />

ACS<br />

Fig. 1 p66Shc mRNA expression, relative to expression of 18S rRNA,<br />

in peripheral blood monocytes from angiographically confirmed<br />

CAD-free controls, stable CAD patients and patients with ACS.<br />

Fig. 3 Cerebral arteries of young and aged mice in the process of<br />

being homogenized prior to protein analysis.

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