Immunological and Molecular Mechanisms in Myocardial Remodeling and Heart Failure

Cardiovascular disease (CVD) is the leading cause of death globally. Most forms of CVD are associated with inflammation. Atherosclerosis and chronic heart failure are conditions characterized by a chronic non-resolving inflammatory phenotype, while myocardial infarction and stroke, the direct consequences of atherosclerosis, are acute inflammatory conditions. Our main hypothesis is that these inflammatory processes, chronic or acute, directly contribute to the pathogenesis of CVD. During the recent years our group has gradually shift the focus from heart failure to atherosclerosis and obesity and related metabolic disturbances.

By studying how specific components of the inflammatory response affects CVD progression and also how inflammation is initiated, maintained and terminated, our group has the ambitious aim to develop novel strategies for preventing, identifying and treating different forms of CVD and related metabolic disorders.

Our group has a translational research profile. We use experimental mouse models to mimic CVD development and characterize the pathogenic processes involved. In addition, our research approach includes in vitro studies in primary isolated cells from man and mouse, as well as clinical studies in well characterized patients with CVD, examining samples from peripheral blood as well as tissue samples. The ultimate goal is to develop new treatment modalities in CVD and related disorders.

From left: Kuan Yang, Azita Rashidi, Mieke Louwe, Trine Ranheim, Jonas Øgaard, Knut Lauritzen, Maria Belland Olsen and Øystein Sandanger.