The main focus of our research group is to obtain better insight into the relation between genomic instability, DNA repair mechanisms and the aging process in mammals. We are particularly interested in understanding the role of mitochondria and the maintenance of the mitochondrial genome in the aging process.
Our cells are constantly exposed to exogenous and endogenous DNA damaging agents. Exogenous sources of DNA damage include e.g. ultraviolet irradiation from the sun and chemicals in the environment. Endogenous sources include e.g. reactive oxygen species (ROS), which are mainly produced as part of the mitochondrial oxidative phosphorylation process.
If not properly removed, DNA damage can be devastating to normal cell physiology, leading to mutagenesis and/or cell death. A number of mechanisms have evolved to cope with endogenous or exogenous stress to prevent chromosomal instability and maintain cellular homeostasis. Thus, DNA repair is a very important mechanism for maintenance of genomic integrity. Some DNA lesions may escape the repair mechanisms, and therefore DNA damage and mutations of different types accumulate with age. The accumulation of DNA damage is thought to play a critical role in the aging process, but many open questions remain to be answered regarding how these intricate mechanisms work and influence our health.
In our research projects we are using various aging model systems such as cell lines established from patients suffering from premature aging syndromes and genetically modified mice of various ages.
Using state of the art technologies we study the molecular biology and metabolism of mitochondria in human and mouse tissues and cell lines, and we perform biochemical analysis of proteins that are believed to be involved in genome maintenance.
Our research group also investigates potential correlations between DNA repair capacities in lymphocytes isolated from blood samples of young and old individuals and physiological measures of healthy aging.