Mieke C. Louwe
- Assisting group leader, Postdoc; PhD
- +47 23 07 36 26
Atherosclerosis and related cardiovascular disease are characterized by narrowing of the larger arteries, supplying oxygen rich blood to the body. Narrowing of these arteries usually is caused by fatty deposits: atherosclerotic plaques. In severely narrowed arteries, tiny pieces of plaque can break off and could end up in the heart or the brain, causing a myocardial infarction or stroke, respectively. This might result in death, but especially in those who survive heart failure, in case of a myocardial infarction, or chronic disability, in case of stroke, illustrate the large consequences for these patients. Since the development of the atherosclerotic plaque in a body starts early in life, and progresses over time, it makes almost the whole population vulnerable for possible consequences of this disease.
Atherosclerosis is characterized by chronic inflammation, as indicated by the presence of a variety of immune cells in, or nearby, the atherosclerotic plaque or affected area. Activation of the complement pathway during atherosclerosis appears to be tightly linked to the progression of atherosclerotic plaques. The traditional view of complement as being mainly a host defense system against microbes has evolved markedly the last decades. The current view places complement as a surveillance system that quickly can be activated by sensing any danger to the host and thereby contributing to maintain tissue homeostasis and promote repair. On the other hand, undesired or uncontrolled activation of the system can induce tissue damage and organ dysfunction to the host. In this respect complement mediated inflammation is a very interesting research area and treatment target in atherosclerosis and related cardiovascular diseases.
Hence, I investigate in my postdoc project the role the complement system, toll-like receptors, and some other innate immune markers, play in the development of carotid atherosclerosis and stroke, by using 1) various materials from carotid atherosclerotic patient populations and 2) different experimental models.