Bachelor and Master projects

Due to the profound advances in cancer therapy the last decades, the number of cancer survivors is increasing. Adverse cardiac side-effects such as heart failure, may however reduce the quality of life of many survivors and may even halter ongoing cancer therapy. Prevention strategies to reduce cancer therapy-induced cardiotoxicities have been attempted, but many have failed to demonstrate reliable effectiveness. Metabolic remodeling is well described in several forms of heart failure, often preceding the development of impaired cardiac function. The effects of cancer therapy on myocardial metabolism are however largely unknown. As cancer-cells are very different in terms of metabolism and substrate utilization compared to the highly oxidative beating heart cells, metabolic modulation could be a potential therapeutic target for reducing cardiac side-effects associated with cancer therapy.

In the CARETOX project we seek to elucidate how myocardial substrate utilization, lipid-dynamics, mitochondrial fitness, and cardiac inflammation are influenced by anti-cancer treatment.

An improved understanding of the underlying mechanisms can be used to provide better information to healthcare workers, patients and family, and may lead to the development of better prevention and treatment of such side-effects. Ultimately, the research in the CARETOX project has the potential to improve long-term cardiovascular outcomes and quality of life for breast cancer survivors and lead the way for new therapeutic approaches.

Fatty liver is a silent manifestation of the metabolic syndrome that affects millions worldwide leading to metabolic-associated fatty liver disease (MAFLD). Fatty liver is associated with overweight but also increasingly detected in lean individuals and post-menopausal women. Numerous studies have shown fatty liver to be a risk factor for diastolic dysfunction and has a 50% prevalence during HFpEF (heart failure with preserved ejection factor). In fact the risk of cardiac mortality is twice as much as liver-related death in these individuals. The relationship between diabetes with cardiovascular disease has been a major focus at our research group over many years and emphasizes that HFpEF is not an isolated cardiac disorder but is linked to other comorbidities including fatty liver.

This project aims to elucidate liver-heart crosstalk following chronic fructose consumption and during HFpEF progression. 

We are currently recruiting MSc and BSc students to work within this project!

The failing heart undergoes structural cardiac remodeling, impaired excitation–contraction (EC) coupling, and metabolic substrate utilization, which consequently induces energetic deficit and oxidative stress. Mitochondria play a central role in many of these processes because they are the main source of cellular ATP, in addition to reactive oxygen species (ROS). Mitochondrial function is critically controlled by calcium. Thus, calcium homeostasis within the myocardium is essential both for contraction but also to modulate ATP production to ensure the homeostasis of energy demand and supply. Disruption of the t-tubules, and mitochondrial uptake of calcium, may play a causative role in driving impaired mitochondrial function and energy metabolism in heart failure. Recent evidence has indicated that the assembly of mitochondrial supercomplexes are important for maintaining efficient respiration and lowering ROS production in the mitochondria and their assembly may be disrupted in heart failure. However whether this is related to energetic deficit in the heart remains to be fully understood. 

We are currently recruiting MSc and BSc students to work within this project!