Translational Cardiology (@TransCardio) – Research group Magnus Bäck

Our research is focused on inflammation in a broad spectrum of cardiovascular diseases, covering for example valvular heart disease, atherosclerosis, coronary artery disease, and arterial stiffness. Our vision is to identify novel mechanisms of cardiovascular disease to be rapidly translated into cardiology clinical practice.

TransCardio Research Areas

Valvular and Vascular Biology

Atherosclerosis

Atherosclerosis is a chronic inflammatory process triggered by accumulation of cholesterol-containing low-density lipoproteins (LDL) particles in the arterial wall. Major etiological factors include hyperlipidemia, hypertension, diabetes, and cigarette smoking, all of which are thought to initiate and promote vascular inflammation.

We study several aspects of atherosclerosis to identify key pathways and targets with therapeutic potential. Our studies in this field range from experimental models to epidemiological and biomarker studies. One focus pathway for our studies is the lipid mediators of inflammation and its resolution.

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Valvular Heart Disease

The heart valves, which maintain a unidirectional cardiac blood flow, are covered by endothelial cells, and structurally composed by valvular interstitial cells and extracellular matrix. Valvular heart disease can be either stenotic, causing obstruction of the valvular flow, or regurgitant referring to a back-flow through the valve. The pathophysiological changes in valvular heart disease include for example lipid and inflammatory cell infiltration, calcification, neoangiogenesis, and extracellular matrix remodelling.

Our research on valvular heart disease span from molecular and cellular studies of valves and valve-derived cells to echocardiography research, biomarkers, and epidemiology.

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Cardiovascular Calcification

Arterial and valvular calcifications become more predominant with aging and may be associated with atherosclerosis and prevalent cardiovascular risk factors. Calcium phosphate precipitations promote a phenotypic shift in vascular smooth muscle and valvular interstitial cells toward an expression pattern of osteoblastic genes, which promote the active phase of mineralization. A line of defense systems protects arterial and valvular calcification. Given the major roles of phosphate in soft tissue calcification, phosphate mimetics and/or prevention of phosphate dissipation represent novel potential therapeutic approaches for arterial and valvular calcification.

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Gastro-cardiology

The cardiovascular risk factor chronic systemic inflammation may reflect gastroenterological inflammatory conditions, such as inflammatory bowel disease and gastrointestinal infections, in particular, chronic Helicobacter pylori infection. Diagnosing and treating Helicobacter pylori to reduce the risk of cardiovascular events and gastrointestinal bleeding are currently under investigation. We have in addition shown that virulence factors carried by Helicobacter pylori are associated with smooth muscle cell calcification.

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Resolution of Cardiovascular Inflammation

An appropriate immune response is crucial for protecting us against harmful stimuli, whereas a maladaptive immune response ultimately causes harm. Dysregulated chronic inflammation with a failure in the resolution of inflammation lead to persistent recruitment and activation of leukocyte subtypes, which fail to skew the immune response to adequate healing of the inflammatory site and for re-establishment of cardiovascular homeostasis. This resolution of inflammation is an active process of limiting inflammatory cell infiltration and favouring phagocytosis and efferocytosis for the removal of debris and apoptotic cells from the site of inflammation.

Resolution of atherosclerosis inflammation

Lipid mediators of inflammation are part of the effectors in the atherosclerotic immune activation However, there are also lipid mediators with the opposite action of limiting and terminating the atherosclerotic inflammation. In particular, the lipid mediators lipoxins and resolvins act as inflammation stop signals by actively promoting the resolution of inflammation. Translational Cardiology is focusing on the GPR18, GPR32, ChemR23, and LXA receptors for these proresolving lipid mediators to decipher their pharmacology and signalling pathways, in particular in atherosclerosis.

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Systemic Inflammation

Our studies on inflammatory biomarkers and the effects of systemic inflammation in relation to cardiovascular disease measures provide important information on the mechanisms behind how chronic inflammation and its failure to resolve contribute to cardiovascular disease.

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Immunomodulation and Cardiovascular Consequences in COVID-19

Translational Cardiology has translated active resolution of inflammation without immunosuppression to application in COVID-19. In a randomized controlled clinical trial performed by Translational Cardiology, omega-3 treatment through intravenous fish oil administration activated metabolic pathways towards lipid proresolving mediators. We also address the vascular effects associated with COVID-19 infection and its chronic consequences.

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Cardiovascular Risk and Prevention

Arterial stiffness

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Omega-3 fatty acids

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Publications

Selected publications

Funding

  • The Swedish Research Council (Vetenskapsrådet)
  • Swedish Heart-Lung Foundation
  • Karolinska Institutet
  • European Union

Members and contact

Group leader

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