Martin Magnusson

Our research

The core my groups research is to bridge the surprisingly under-explored gap between the “omics” of epidemiology (e.g., genomics, metabolomics, proteomics and target biomarkers) and biological and clinical function. Thus, a major component of my research aims to enhance the understanding of causes to progressing diabetes and cardiovascular disease/heart failure where I together with my co-workers, invest large efforts in metabolomics and proteomics as well as target biomarkers. However, a central issue is that we do not stop at finding biomarkers associated with risk of progressing disease, but also examine the importance of genetic predisposition behind such relationship to find causal association and we also aim to explore the underlying mechanisms (by in vivo/vitro experiments and even human trials if applicable).

As an example of this we have recently reported that in two prospective, community-based studies, elevated levels of the gut hormone (incretin) glucose-dependent insulinotropic peptide (GIP) were associated with greater risk of all-cause and cardiovascular mortality within 5–9 years of follow-up and that bi-directional Mendelian randomization analyses provided evidence of GIPs causal involvement in cardiovascular disease implicating that stimulation of the GIP receptor indeed could be harmful. We are currently undertaking additional human and animal studies to investigate the possible harmful effects of GIP further in a translational fashion within the WCMM framework, read more.

As a further example of the drug target research undertaken in my group, we have in epidemiological studies identified deficiency of the basic element selenium to be associated with marked worse prognosis in patients with heart failure. These findings have later been replicated in other European heart failure cohorts. Notable, severe Selenium deficiency in humans is associated with a rare but fatal form of HF that is restricted to specific geographic regions (Keshan disease) with very low amount of Selenium in the soil and thus in food. Keshan disease is reversible with Selenium supplementation, indicating the potential causative role of Selenium deficiency in inducing heart failure in these patients. The current evidence is not (yet) strong enough to encourage Selenium supplementation in a clinical practice. It is, however, encouraging enough to start large well-designed randomized clinical trials, which we are currently planning for in a big Swedish multicentre register-based RCT (Magnusson PI).

Aims

• To identify novel drugs targets for the treatment of diabetes, cardiovascular disease and heart failure

Strengths of the group

A major strength of the group is a long-standing experience of conducting large epidemiological studies in some of the largest population-based cohorts in the world. However, a central issue is that we do not stop at finding metabolites/proteins/biomarkers and metabolomics/proteomic/biomarkers patterns associated with risk of progressing disease, but we also examine the importance of genetic predisposition behind such relationship to find causal association and we also aim to explore the underlying mechanisms (by in vivo/vitro experiments and even human trials if applicable). When identifying a possible drug target, we then proceed to undertake RCT (as for the case of selenium).

Impact

| Research Output

Affiliations

• Wallenberg Center for Molecular Medicine 
• Department of Cardiology, Skåne University Hospital, Malmö
• Department of Clinical Sciences, Lund University, Skåne University Hospital, Malmö
• Hypertension in Africa Research Team (HART); North-West University, Potchefstroom, South Africa

Social media

• ResearchGate