Growing epidemiological evidence indicates an excess risk of late occurring cardiovascular diseases (CVD) at much lower doses of ionizing radiation than previously thought. Until now, these epidemiological data are suggestive rather than persuasive due to a lack of statistical power and fairly limited knowledge of the underlying biological and molecular mechanisms. As a result, cardiovascular effects of low dose ionizing radiation still constitute a black box resulting in a possible improper radiation protection. In this project we will focus on atherosclerosis as a possible mechanism of radiation-induced CVD.

Description

This research proposal focuses at characterizing and targeting intercellular signaling mechanisms in vitro and in vivo that modulate EC damage which strongly links to the onset and development of atherosclerosis.

The following objectives will be addressed:
Do Cxs and their channels contribute to radiation-induced cell death/inflammatory responses in ECs in vitro and in vivo?
Is the ROS/Ca2+ signaling axis a central player in the radiation-induced cell death/inflammatory responses in ECs in vitro?
Are Cx-mediated Ca2+ waves involved in the cell-cell propagation of ROS production?

Nr of positions available : 1

Research Fields

Engineering

Career Stage

Early stage researcher or 0-4 yrs (Post graduate)

Research Profiles

First Stage Researcher (R1)