• About
Karolinska institutet
Karolinska universitetssjukhuset

Magnus Bäck Group

Translational Cardiology


Follow on X (formerly called Twitter):@TransCardio

Research in Magnus Bäck’s group Translational Cardiology (@TransCardio) is focused on inflammation in a broad spectrum of cardiovascular diseases, covering for example valvular heart disease, atherosclerosis, coronary artery disease, and arterial stiffness.

Translational Cardiology’s vision is to identify novel mechanisms of cardiovascular disease to be rapidly translated into cardiology clinical practice.

Magnus Bäck is Senior Consultant and Professor of Cardiology. He is serving as the Director of Cardiovascular Research and Education at the Karolinska University Hospital and. His present work combines clinical cardiology in coronary and valvular heart disease with translational research on atherosclerosis, aortic valve stenosis, and cardiovascular risk factors, with emphasis on the role of inflammation. Professor Bäck is the Editor in Chief of two journals published by the European Society of Cardiology; ESC-Heart Failure and European Heart Journal Open.

Valvular and vascular biology

TransCardio – Valvular and Vascular Biology


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.


Translational opportunities of single-cell biology in atherosclerosis.

The resolvin D1 receptor GPR32 transduces inflammation resolution and atheroprotection.

Inflammation and its resolution in atherosclerosis: mediators and therapeutic opportunities.

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 remodeling.

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


rtificial Intelligence Models Reveal Sex-Specific Gene Expression in Aortic Valve Calcification.

The tyrosine kinase inhibitor nilotinib targets the discoidin domain receptor DDR2 in calcific aortic valve stenosis.

Omega-3 Polyunsaturated Fatty Acids Decrease Aortic Valve Disease Through the Resolvin E1 and ChemR23 Axis.

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 protect 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.


rom organic and inorganic phosphates to valvular and vascular calcifications.

Omega-3 Polyunsaturated Fatty Acids Decrease Aortic Valve Disease Through the Resolvin E1 and ChemR23 Axis.

The G-protein coupled receptor ChemR23 determines smooth muscle cell phenotypic switching to enhance high phosphate-induced vascular calcification.



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.


Helicobacter Pylori Virulence Factor Cytotoxin-Associated Gene A (CagA) Induces Vascular Calcification in Coronary Artery Smooth Muscle Cells.

Gastro-Cardiology: A Novel Perspective for the Gastrocardiac Syndrome.

Helicobacter pylori screening in clinical routine during hospitalization for acute myocardial infarction.

Resolution of inflammation

TransCardio – 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 favoring 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 emdiators 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 signaling pathways in particular in atherosclerosis.


The resolvin D2 – GPR18 axis is expressed in human coronary atherosclerosis and transduces atheroprotection in apolipoprotein E deficient mice.

The resolvin D1 receptor GPR32 transduces inflammation resolution and atheroprotection.

ERV1/ChemR23 Signaling Protects Against Atherosclerosis by Modifying Oxidized Low-Density Lipoprotein Uptake and Phagocytosis in Macrophages.

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.


Omega-3 to omega-6 fatty acid oxidation ratio as a novel inflammation resolution marker for metabolic complications in obesity.

Antiphospholipid antibodies in patients with calcific aortic valve stenosis.

Cardiovascular Autonomic Function Changes and Predictors During a 2-Year Physical Activity Program in Rheumatoid Arthritis: A PARA 2010 Substudy.

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.


Immunomodulation by intravenous omega-3 fatty acid treatment in older subjects hospitalized for COVID-19: A single-blind randomized controlled trial.

Decreased oxidative stress and altered urinary oxylipidome by intravenous omega-3 fatty acid emulsion in a randomized controlled trial of older subjects hospitalized for COVID-19.

Endothelial dysfunction in COVID-19: a position paper of the ESC Working Group for Atherosclerosis and Vascular Biology, and the ESC Council of Basic Cardiovascular Science.

Group Leader

Magnus Bäck, Professor, magnus.back@ki.se

Group members

Sven-Christian Pawelzik, Team Leader, sven-christian.pawelzik@ki.se

Luis Miguel Cardoso Dos Santos, Postdoc, luis.santos@ki.se

Oscar Plunde, Postdoc, oscar.persson@ki.se

David Hupin, Postdoc, david.hupin@ki.se

Philip Sarajlic, PhD student, philip.sarajlic@ki.se

Simin Zhang, PhD student, simin.zhang.2@ki.se

Zihan Qin, PhD student, zihan.qin@ki.se

Mohammed Hashem, PhD student, mohammed.hashem@ki.se

Luke Flannery, student, luke.flannery@ki.se

Bahration Borovskyi, student, bahration.borovskyi@stud.ki.se

About CMM

The Center for Molecular Medicine (CMM) is a foundation instituted by the Stockholm County Council (Region Stockholm). CMM is at the heart of a close partnership with the Karolinska University Hospital and Karolinska Institutet, fueling advancements in biomedical and clinical research.


Center for Molecular Medicine Foundation, org. nr. 815201-3689

Karolinska University Hospital L8:05

Visionsgatan 18

171 76 Stockholm, Sweden


Karolinska institutet
Karolinska universitetssjukhuset