This page has only limited features, please log in for full access.

Prof. Magnus Bäck
Karolinska Institutet, Stockholm, Sweden

Basic Info


Research Keywords & Expertise

0 Atherosclerosis
0 Cardiology
0 Echocardiography
0 Inflammation
0 Valvular heart disease

Fingerprints

Atherosclerosis
Inflammation
Cardiology
Valvular heart disease
Echocardiography

Honors and Awards

The user has no records in this section


Career Timeline

The user has no records in this section.


Short Biography

The user biography is not available.
Following
Followers
Co Authors
The list of users this user is following is empty.
Following: 0 users

Feed

Journal article
Published: 23 August 2021 in European Heart Journal - Cardiovascular Pharmacotherapy
Reads 0
Downloads 0

Aims Of all spontaneous bleeding complications in patients with acute myocardial infarction (MI), upper gastrointestinal bleeding (UGIB) is common and of specific interest since it could be prevented by several prophylactic measures. We aimed to determine the incidence, associated outcomes, and predictors of UGIB following acute MI. Methods and results All patients with acute MI enrolled in the SWEDEHEART (Swedish Web-system for Enhancement and Development of Evidence-based care in Heart disease Evaluated According to Recommended Therapies) registry from January 2007 to June 2016 and discharged alive on any antithrombotic therapy (n = 149 477) were followed regarding UGIB for 1 year. Associated outcomes were determined by Cox proportional hazards regression with UGIB as a time-dependent covariate, adjusting for baseline characteristics, invasive treatment, and medical treatment at discharge. Predictors of UGIB were determined by logistic regression and machine learning models. At 1 year, UGIB had occurred in 2230 patients (cumulative incidence 1.5%) and was significantly associated with an increased risk of all-cause death [hazard ratio (HR) 2.86, 95% confidence interval (CI) 2.58–3.16] and stroke (HR 1.80, 95% CI 1.32–2.45) but not with recurrent MI (HR 1.17, 95% CI 0.97–1.42). The most important predictors of UGIB were haemoglobin, age, systolic blood pressure, blood glucose, smoking status, previous upper gastrointestinal bleeding, and antithrombotic and gastroprotective treatment. Conclusion After acute MI, readmission because of UGIB is common and significantly associated with poor prognosis. By using machine learning in addition to traditional logistic regression, new predictors of UGIB, such as blood glucose and smoking status, were identified.

ACS Style

Philip Sarajlic; Moa Simonsson; Tomas Jernberg; Magnus Bäck; Robin Hofmann. Incidence, associated outcomes, and predictors of upper gastrointestinal bleeding following acute myocardial infarction: a SWEDEHEART-based nationwide cohort study. European Heart Journal - Cardiovascular Pharmacotherapy 2021, 1 .

AMA Style

Philip Sarajlic, Moa Simonsson, Tomas Jernberg, Magnus Bäck, Robin Hofmann. Incidence, associated outcomes, and predictors of upper gastrointestinal bleeding following acute myocardial infarction: a SWEDEHEART-based nationwide cohort study. European Heart Journal - Cardiovascular Pharmacotherapy. 2021; ():1.

Chicago/Turabian Style

Philip Sarajlic; Moa Simonsson; Tomas Jernberg; Magnus Bäck; Robin Hofmann. 2021. "Incidence, associated outcomes, and predictors of upper gastrointestinal bleeding following acute myocardial infarction: a SWEDEHEART-based nationwide cohort study." European Heart Journal - Cardiovascular Pharmacotherapy , no. : 1.

Journal article
Published: 01 August 2021 in European Heart Journal Open
Reads 0
Downloads 0

The Editorial Board of European Heart Journal Open (EHJ Open) has unlocked the doors to open science in cardiology—#OpenUpYourScience. EHJ Open is designed to facilitate fluid and open communication between all subject sections in cardiology, with the aim of achieving open and interactive science for a broad readership (Figure 1). EHJ Open is an open house for all researchers, readers, practitioners, and allied professionals in cardiology. The section editors consolidate to allow an accelerated and global sharing of high-quality science on all aspects of cardiovascular disease (CVD).

ACS Style

Magnus Bäck; Maciej Banach; Frieder Braunschweig; Salvatore De Rosa; Alessia Gimelli; Thomas Kahan; Daniel F J Ketelhuth; Patrizio Lancellotti; Susanna C Larsson; Linda Mellbin; Edit Nagy; Gianluigi Savarese; Karolina Szummer; Denis Wahl; European Heart Journal Open Section Editors. Open Up your Science in EHJ Open. European Heart Journal Open 2021, 1, 1 .

AMA Style

Magnus Bäck, Maciej Banach, Frieder Braunschweig, Salvatore De Rosa, Alessia Gimelli, Thomas Kahan, Daniel F J Ketelhuth, Patrizio Lancellotti, Susanna C Larsson, Linda Mellbin, Edit Nagy, Gianluigi Savarese, Karolina Szummer, Denis Wahl, European Heart Journal Open Section Editors. Open Up your Science in EHJ Open. European Heart Journal Open. 2021; 1 (1):1.

Chicago/Turabian Style

Magnus Bäck; Maciej Banach; Frieder Braunschweig; Salvatore De Rosa; Alessia Gimelli; Thomas Kahan; Daniel F J Ketelhuth; Patrizio Lancellotti; Susanna C Larsson; Linda Mellbin; Edit Nagy; Gianluigi Savarese; Karolina Szummer; Denis Wahl; European Heart Journal Open Section Editors. 2021. "Open Up your Science in EHJ Open." European Heart Journal Open 1, no. 1: 1.

Editorial
Published: 06 July 2021 in Atherosclerosis
Reads 0
Downloads 0

Oxidative stress orchestrates atherosclerosis through lipoprotein modifications, heightened inflammation, and effects on cell death and function. The oxidative stress levels are tightly regulated through alterations in the reactive oxygen species (ROS) production and degradation systems. The bidirectional alterations of these systems in the vascular wall reflects both causative and defensive processes during atherogenesis.

ACS Style

Nathalie Mercier; Magnus Bäck. The double-action of hydrogen peroxide on the oxidative atherosclerosis battlefield. Atherosclerosis 2021, 1 .

AMA Style

Nathalie Mercier, Magnus Bäck. The double-action of hydrogen peroxide on the oxidative atherosclerosis battlefield. Atherosclerosis. 2021; ():1.

Chicago/Turabian Style

Nathalie Mercier; Magnus Bäck. 2021. "The double-action of hydrogen peroxide on the oxidative atherosclerosis battlefield." Atherosclerosis , no. : 1.

Journal article
Published: 25 June 2021 in IUPHAR/BPS Guide to Pharmacology CITE
Reads 0
Downloads 0

The formylpeptide receptors (nomenclature agreed by the NC-IUPHAR Subcommittee on the formylpeptide receptor family [196]) respond to exogenous ligands such as the bacterial product fMet-Leu-Phe (fMLP) and endogenous ligands such as lipoxin A4 (LXA4), 15-epi-lipoxin A4, annexin I , cathepsin G, amyloid β42, serum amyloid A and spinorphin, derived from β-haemoglobin. FPR1 also serves as a plague receptor for selective destruction of human immune cells by Y. pestis [135]. The FPR1/2 agonists 'compound 17b' and 'compound 43' have shown cardiac protective functions [149, 64].

ACS Style

Magnus Bäck; François Boulay; Nan Chiang; Sven-Erik Dahlén; Claes Dahlgren; Jeffrey Drazen; Jilly F. Evans; Craig Gerard; Philip M. Murphy; Marc Parmentier; Mark Quinn; G. Enrico Rovati; Charles N. Serhan; Takao Shimizu; Ji Ming Wang; Richard D. Ye; Takehiko Yokomizo. Formylpeptide receptors in GtoPdb v.2021.2. IUPHAR/BPS Guide to Pharmacology CITE 2021, 2021, 1 .

AMA Style

Magnus Bäck, François Boulay, Nan Chiang, Sven-Erik Dahlén, Claes Dahlgren, Jeffrey Drazen, Jilly F. Evans, Craig Gerard, Philip M. Murphy, Marc Parmentier, Mark Quinn, G. Enrico Rovati, Charles N. Serhan, Takao Shimizu, Ji Ming Wang, Richard D. Ye, Takehiko Yokomizo. Formylpeptide receptors in GtoPdb v.2021.2. IUPHAR/BPS Guide to Pharmacology CITE. 2021; 2021 (2):1.

Chicago/Turabian Style

Magnus Bäck; François Boulay; Nan Chiang; Sven-Erik Dahlén; Claes Dahlgren; Jeffrey Drazen; Jilly F. Evans; Craig Gerard; Philip M. Murphy; Marc Parmentier; Mark Quinn; G. Enrico Rovati; Charles N. Serhan; Takao Shimizu; Ji Ming Wang; Richard D. Ye; Takehiko Yokomizo. 2021. "Formylpeptide receptors in GtoPdb v.2021.2." IUPHAR/BPS Guide to Pharmacology CITE 2021, no. 2: 1.

Reference work
Published: 13 June 2021 in Encyclopedia of Molecular Pharmacology
Reads 0
Downloads 0
ACS Style

Hildur Arnardottir; Magnus Bäck. Pro-resolving Mediators. Encyclopedia of Molecular Pharmacology 2021, 1 -6.

AMA Style

Hildur Arnardottir, Magnus Bäck. Pro-resolving Mediators. Encyclopedia of Molecular Pharmacology. 2021; ():1-6.

Chicago/Turabian Style

Hildur Arnardottir; Magnus Bäck. 2021. "Pro-resolving Mediators." Encyclopedia of Molecular Pharmacology , no. : 1-6.

Corrected proof
Published: 09 February 2021 in Cardiovascular Research
Reads 0
Downloads 0

Calcification of the arterial wall and valves is an important part of the pathophysiological process of peripheral and coronary atherosclerosis, aortic stenosis, ageing, diabetes, and chronic kidney disease. This review aims to better understand how extracellular phosphates and their ability to be retained as calcium phosphates on the extracellular matrix initiate the mineralization process of arteries and valves. In this context, the physiological process of bone mineralization remains a human model for pathological soft tissue mineralization. Soluble (ionized) calcium precipitation occurs on extracellular phosphates; either with inorganic or on exposed organic phosphates. Organic phosphates are classified as either structural (phospholipids, nucleic acids) or energetic (corresponding to phosphoryl transfer activities). Extracellular phosphates promote a phenotypic shift in vascular smooth muscle and valvular interstitial cells towards an osteoblast gene expression pattern, which provokes the active phase of mineralization. A line of defense systems protects arterial and valvular tissue calcifications. 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.

ACS Style

Magnus Bäck; Jean-Baptiste Michel. From organic and inorganic phosphates to valvular and vascular calcifications. Cardiovascular Research 2021, 117, 2016 -2029.

AMA Style

Magnus Bäck, Jean-Baptiste Michel. From organic and inorganic phosphates to valvular and vascular calcifications. Cardiovascular Research. 2021; 117 (9):2016-2029.

Chicago/Turabian Style

Magnus Bäck; Jean-Baptiste Michel. 2021. "From organic and inorganic phosphates to valvular and vascular calcifications." Cardiovascular Research 117, no. 9: 2016-2029.

Mini review article
Published: 11 January 2021 in Frontiers in Physiology
Reads 0
Downloads 0

Infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes coronavirus disease 2019 (COVID-19). SARS-CoV-2 triggers an immune response with local inflammation in the lung, which may extend to a systemic hyperinflammatory reaction. Excessive inflammation has been reported in severe cases with respiratory failure and cardiovascular complications. In addition to the release of cytokines, referred to as cytokine release syndrome or “cytokine storm,” increased pro-inflammatory lipid mediators derived from the omega-6 polyunsaturated fatty acid (PUFA) arachidonic acid may cause an “eicosanoid storm,” which contributes to the uncontrolled systemic inflammation. Specialized pro-resolving mediators, which are derived from omega-3 PUFA, limit inflammatory reactions by an active process called resolution of inflammation. Here, the rationale for omega-3 PUFA supplementation in COVID-19 patients is presented along with a brief overview of the study protocol for the trial “Resolving Inflammatory Storm in COVID-19 Patients by Omega-3 Polyunsaturated Fatty Acids - A single-blind, randomized, placebo-controlled feasibility study” (COVID-Omega-F). EudraCT: 2020-002293-28; clinicaltrials.gov: NCT04647604.

ACS Style

Hildur Arnardottir; Sven-Christian Pawelzik; Ulf Öhlund Wistbacka; Gonzalo Artiach; Robin Hofmann; Ingalill Reinholdsson; Frieder Braunschweig; Per Tornvall; Dorota Religa; Magnus Bäck. Stimulating the Resolution of Inflammation Through Omega-3 Polyunsaturated Fatty Acids in COVID-19: Rationale for the COVID-Omega-F Trial. Frontiers in Physiology 2021, 11, 624657 .

AMA Style

Hildur Arnardottir, Sven-Christian Pawelzik, Ulf Öhlund Wistbacka, Gonzalo Artiach, Robin Hofmann, Ingalill Reinholdsson, Frieder Braunschweig, Per Tornvall, Dorota Religa, Magnus Bäck. Stimulating the Resolution of Inflammation Through Omega-3 Polyunsaturated Fatty Acids in COVID-19: Rationale for the COVID-Omega-F Trial. Frontiers in Physiology. 2021; 11 ():624657.

Chicago/Turabian Style

Hildur Arnardottir; Sven-Christian Pawelzik; Ulf Öhlund Wistbacka; Gonzalo Artiach; Robin Hofmann; Ingalill Reinholdsson; Frieder Braunschweig; Per Tornvall; Dorota Religa; Magnus Bäck. 2021. "Stimulating the Resolution of Inflammation Through Omega-3 Polyunsaturated Fatty Acids in COVID-19: Rationale for the COVID-Omega-F Trial." Frontiers in Physiology 11, no. : 624657.

Mini review
Published: 12 November 2020 in Frontiers in Cell and Developmental Biology
Reads 0
Downloads 0

Inflammation is well-established in cardiovascular disease, including valvular heart disease. Inflammation is a key process in the fibrosis and calcification of the aortic valve leaflets, which ultimately clinically manifest as aortic valve stenosis characterized by valve dysfunction and cardiac obstruction. In the absence of pharmacological treatment, either surgical or transcatheter aortic valve replacement is currently the only available therapeutic strategy for patients with severe aortic valve stenosis. Omega-3 polyunsaturated fatty acids, which exert beneficial effects in several cardiovascular diseases, serve as the substrate for several bioactive lipid mediators that regulate inflammation. Recent findings point to the beneficial effects of omega-3 fatty acids in cardiac valves, being inversely associated with aortic valve calcification and contributing to the resolution of valvular inflammation by means of the pro-resolving mediator resolvin E1 and downstream signaling through its receptor ChemR23.

ACS Style

Gonzalo Artiach; Magnus Bäck. Omega-3 Polyunsaturated Fatty Acids and the Resolution of Inflammation: Novel Therapeutic Opportunities for Aortic Valve Stenosis? Frontiers in Cell and Developmental Biology 2020, 8, 1 .

AMA Style

Gonzalo Artiach, Magnus Bäck. Omega-3 Polyunsaturated Fatty Acids and the Resolution of Inflammation: Novel Therapeutic Opportunities for Aortic Valve Stenosis? Frontiers in Cell and Developmental Biology. 2020; 8 ():1.

Chicago/Turabian Style

Gonzalo Artiach; Magnus Bäck. 2020. "Omega-3 Polyunsaturated Fatty Acids and the Resolution of Inflammation: Novel Therapeutic Opportunities for Aortic Valve Stenosis?" Frontiers in Cell and Developmental Biology 8, no. : 1.

Journal article
Published: 04 September 2020 in European Heart Journal - Cardiovascular Imaging
Reads 0
Downloads 0

Atherosclerotic plaques prone to rupture may cause acute myocardial infarction (MI) but can also heal without causing an event. Certain common histopathological features, including inflammation, a thin fibrous cap, positive remodelling, a large necrotic core, microcalcification, and plaque haemorrhage are commonly found in plaques causing an acute event. Recent advances in imaging techniques have made it possible to detect not only luminal stenosis and overall coronary atherosclerosis burden but also to identify such adverse plaque characteristics. However, the predictive value of identifying individual adverse atherosclerotic plaques for future events has remained poor. In this Position Paper, the relationship between vulnerable plaque imaging and MI is addressed, mainly for non-invasive assessments but also for invasive imaging of adverse plaques in patients undergoing invasive coronary angiography. Dynamic changes in atherosclerotic plaque development and composition may indicate that an adverse plaque phenotype should be considered at the patient level rather than for individual plaques. Imaging of adverse plaque burden throughout the coronary vascular tree, in combination with biomarkers and biomechanical parameters, therefore holds promise for identifying subjects at increased risk of MI and for guiding medical and invasive treatment.

ACS Style

Marc R Dweck; Pál Maurovich-Horvat; Tim Leiner; Bernard Cosyns; Zahi A Fayad; Frank J H Gijsen; Kim Van Der Heiden; M Eline Kooi; Akiko Maehara; James E Muller; David E Newby; Jagat Narula; Gianluca Pontone; Evelyn Regar; Patrick W Serruys; Antonius F W Van Der Steen; Peter H Stone; Johannes L Waltenberger; Chun Yuan; Paul C Evans; Esther Lutgens; Jolanda J Wentzel; Magnus Bäck. Contemporary rationale for non-invasive imaging of adverse coronary plaque features to identify the vulnerable patient: a Position Paper from the European Society of Cardiology Working Group on Atherosclerosis and Vascular Biology and the European Association of Cardiovascular Imaging. European Heart Journal - Cardiovascular Imaging 2020, 21, 1177 -1183.

AMA Style

Marc R Dweck, Pál Maurovich-Horvat, Tim Leiner, Bernard Cosyns, Zahi A Fayad, Frank J H Gijsen, Kim Van Der Heiden, M Eline Kooi, Akiko Maehara, James E Muller, David E Newby, Jagat Narula, Gianluca Pontone, Evelyn Regar, Patrick W Serruys, Antonius F W Van Der Steen, Peter H Stone, Johannes L Waltenberger, Chun Yuan, Paul C Evans, Esther Lutgens, Jolanda J Wentzel, Magnus Bäck. Contemporary rationale for non-invasive imaging of adverse coronary plaque features to identify the vulnerable patient: a Position Paper from the European Society of Cardiology Working Group on Atherosclerosis and Vascular Biology and the European Association of Cardiovascular Imaging. European Heart Journal - Cardiovascular Imaging. 2020; 21 (11):1177-1183.

Chicago/Turabian Style

Marc R Dweck; Pál Maurovich-Horvat; Tim Leiner; Bernard Cosyns; Zahi A Fayad; Frank J H Gijsen; Kim Van Der Heiden; M Eline Kooi; Akiko Maehara; James E Muller; David E Newby; Jagat Narula; Gianluca Pontone; Evelyn Regar; Patrick W Serruys; Antonius F W Van Der Steen; Peter H Stone; Johannes L Waltenberger; Chun Yuan; Paul C Evans; Esther Lutgens; Jolanda J Wentzel; Magnus Bäck. 2020. "Contemporary rationale for non-invasive imaging of adverse coronary plaque features to identify the vulnerable patient: a Position Paper from the European Society of Cardiology Working Group on Atherosclerosis and Vascular Biology and the European Association of Cardiovascular Imaging." European Heart Journal - Cardiovascular Imaging 21, no. 11: 1177-1183.

Research article
Published: 25 August 2020 in Circulation
Reads 0
Downloads 0

Background: Aortic valve stenosis (AVS), which is the most common valvular heart disease, causes a progressive narrowing of the aortic valve as a consequence of thickening and calcification of the aortic valve leaflets. The beneficial effects of omega-3 polyunsaturated fatty acids (n-3 PUFAs) in cardiovascular prevention have recently been demonstrated in a large randomized, controlled trial. In addition, n-3 PUFAs serve as the substrate for the synthesis of specialized proresolving mediators, which are known by their potent beneficial anti-inflammatory, proresolving, and tissue-modifying properties in cardiovascular disease. However, the effects of n-3 PUFA and specialized proresolving mediators on AVS have not yet been determined. The aim of this study was to identify the role of n-3 PUFA–derived specialized proresolving mediators in relation to the development of AVS. Methods: Lipidomic and transcriptomic analyses were performed in human tricuspid aortic valves. Apoe −/− mice and wire injury in C57BL/6J mice were used as models for mechanistic studies. Results: We found that n-3 PUFA incorporation into human stenotic aortic valves was higher in noncalcified regions compared with calcified regions. Liquid chromatography tandem mass spectrometry–based lipid mediator lipidomics identified that the n-3 PUFA–derived specialized proresolving mediator resolvin E1 was dysregulated in calcified regions and acted as a calcification inhibitor. Apoe −/− mice expressing the Caenorhabditis elegans Fat-1 transgene (Fat-1 tg ×Apoe −/− ), which enables the endogenous synthesis of n-3 PUFA and increased valvular n-3 PUFA content, exhibited reduced valve calcification, lower aortic valve leaflet area, increased M2 macrophage polarization, and improved echocardiographic parameters. Finally, abrogation of the resolvin E1 receptor ChemR23 enhanced disease progression, and the beneficial effects of Fat-1 tg were abolished in the absence of ChemR23. Conclusions: n-3 PUFA-derived resolvin E1 and its receptor ChemR23 emerge as a key axis in the inhibition of AVS progression and may represent a novel potential therapeutic opportunity to be evaluated in patients with AVS.

ACS Style

Gonzalo Artiach; Miguel Carracedo; Oscar Plunde; Craig E. Wheelock; Silke Thul; Peter Sjövall; Anders Franco-Cereceda; Andres Laguna-Fernandez; Hildur Arnardottir; Magnus Bäck. Omega-3 Polyunsaturated Fatty Acids Decrease Aortic Valve Disease Through the Resolvin E1 and ChemR23 Axis. Circulation 2020, 142, 776 -789.

AMA Style

Gonzalo Artiach, Miguel Carracedo, Oscar Plunde, Craig E. Wheelock, Silke Thul, Peter Sjövall, Anders Franco-Cereceda, Andres Laguna-Fernandez, Hildur Arnardottir, Magnus Bäck. Omega-3 Polyunsaturated Fatty Acids Decrease Aortic Valve Disease Through the Resolvin E1 and ChemR23 Axis. Circulation. 2020; 142 (8):776-789.

Chicago/Turabian Style

Gonzalo Artiach; Miguel Carracedo; Oscar Plunde; Craig E. Wheelock; Silke Thul; Peter Sjövall; Anders Franco-Cereceda; Andres Laguna-Fernandez; Hildur Arnardottir; Magnus Bäck. 2020. "Omega-3 Polyunsaturated Fatty Acids Decrease Aortic Valve Disease Through the Resolvin E1 and ChemR23 Axis." Circulation 142, no. 8: 776-789.

Journal article
Published: 04 August 2020 in Cardiovascular Research
Reads 0
Downloads 0

The COVID-19 pandemic is an unprecedented healthcare emergency causing mortality and illness across the world. Although primarily affecting the lungs, the SARS-CoV-2 virus also affects the cardiovascular system. In addition to cardiac effects, e.g. myocarditis, arrhythmias, and myocardial damage, the vasculature is affected in COVID-19, both directly by the SARS-CoV-2 virus, and indirectly as a result of a systemic inflammatory cytokine storm. This includes the role of the vascular endothelium in the recruitment of inflammatory leucocytes where they contribute to tissue damage and cytokine release, which are key drivers of acute respiratory distress syndrome (ARDS), in disseminated intravascular coagulation, and cardiovascular complications in COVID-19. There is also evidence linking endothelial cells (ECs) to SARS-CoV-2 infection including: (i) the expression and function of its receptor angiotensin-converting enzyme 2 (ACE2) in the vasculature; (ii) the prevalence of a Kawasaki disease-like syndrome (vasculitis) in COVID-19; and (iii) evidence of EC infection with SARS-CoV-2 in patients with fatal COVID-19. Here, the Working Group on Atherosclerosis and Vascular Biology together with the Council of Basic Cardiovascular Science of the European Society of Cardiology provide a Position Statement on the importance of the endothelium in the underlying pathophysiology behind the clinical presentation in COVID-19 and identify key questions for future research to address. We propose that endothelial biomarkers and tests of function (e.g. flow-mediated dilatation) should be evaluated for their usefulness in the risk stratification of COVID-19 patients. A better understanding of the effects of SARS-CoV-2 on endothelial biology in both the micro- and macrovasculature is required, and endothelial function testing should be considered in the follow-up of convalescent COVID-19 patients for early detection of long-term cardiovascular complications.

ACS Style

Paul C Evans; G Ed Rainger; Justin C Mason; Tomasz J Guzik; Elena Osto; Zania Stamataki; Desley Neil; Imo E Hoefer; Maria Fragiadaki; Johannes Waltenberger; Christian Weber; Marie-Luce Bochaton-Piallat; Magnus Bäck. 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. Cardiovascular Research 2020, 116, 2177 -2184.

AMA Style

Paul C Evans, G Ed Rainger, Justin C Mason, Tomasz J Guzik, Elena Osto, Zania Stamataki, Desley Neil, Imo E Hoefer, Maria Fragiadaki, Johannes Waltenberger, Christian Weber, Marie-Luce Bochaton-Piallat, Magnus Bäck. 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. Cardiovascular Research. 2020; 116 (14):2177-2184.

Chicago/Turabian Style

Paul C Evans; G Ed Rainger; Justin C Mason; Tomasz J Guzik; Elena Osto; Zania Stamataki; Desley Neil; Imo E Hoefer; Maria Fragiadaki; Johannes Waltenberger; Christian Weber; Marie-Luce Bochaton-Piallat; Magnus Bäck. 2020. "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." Cardiovascular Research 116, no. 14: 2177-2184.

Journal article
Published: 16 July 2020 in Cells
Reads 0
Downloads 0

Calcific aortic valve stenosis (CAVS) is a common age-related disease characterized by active calcification of the leaflets of the aortic valve. How innate immune cells are involved in disease pathogenesis is not clear. In this study we investigate the role of the pattern recognition receptor Toll-like receptor 7 (TLR7) in CAVS, especially in relation to macrophage subtype. Human aortic valves were used for mRNA expression analysis, immunofluorescence staining, or ex vivo tissue assays. Response to TLR7 agonist in primary macrophages and valvular interstitial cells (VICs) were investigated in vitro. In the aortic valve, TLR7 correlated with M2 macrophage markers on mRNA levels. Expression was higher in the calcified part compared with the intermediate and healthy parts. TLR7+ cells were co-stained with M2-type macrophage receptors CD163 and CD206. Ex vivo stimulation of valve tissue with the TLR7 ligand imiquimod significantly increased secretion of IL-10, TNF-α, and GM-CSF. Primary macrophages responded to imiquimod with increased secretion of IL-10 while isolated VICs did not respond. In summary, in human aortic valves TLR7 expression is associated with M2 macrophages markers. Ex vivo tissue challenge with TLR7 ligand led to secretion of immunomodulatory cytokine IL-10. These results connect TLR7 activation in CAVS to reduced inflammation and improved clearance.

ACS Style

Glykeria Karadimou; Oscar Plunde; Sven-Christian Pawelzik; Miguel Carracedo; Per Eriksson; Anders Franco-Cereceda; Gabrielle Paulsson-Berne; Magnus Bäck. TLR7 Expression is Associated with M2 Macrophage Subset in Calcific Aortic Valve Stenosis. Cells 2020, 9, 1710 .

AMA Style

Glykeria Karadimou, Oscar Plunde, Sven-Christian Pawelzik, Miguel Carracedo, Per Eriksson, Anders Franco-Cereceda, Gabrielle Paulsson-Berne, Magnus Bäck. TLR7 Expression is Associated with M2 Macrophage Subset in Calcific Aortic Valve Stenosis. Cells. 2020; 9 (7):1710.

Chicago/Turabian Style

Glykeria Karadimou; Oscar Plunde; Sven-Christian Pawelzik; Miguel Carracedo; Per Eriksson; Anders Franco-Cereceda; Gabrielle Paulsson-Berne; Magnus Bäck. 2020. "TLR7 Expression is Associated with M2 Macrophage Subset in Calcific Aortic Valve Stenosis." Cells 9, no. 7: 1710.

Journal article
Published: 19 June 2020 in IUPHAR/BPS Guide to Pharmacology CITE
Reads 0
Downloads 0

The leukotriene receptors (nomenclature as agreed by the NC-IUPHAR subcommittee on Leukotriene Receptors [34, 37]) are activated by the endogenous ligands leukotrienes (LT), synthesized from lipoxygenase metabolism of arachidonic acid. The human BLT1 receptor is the high affinity LTB4 receptor whereas the BLT2 receptor in addition to being a low-affinity LTB4 receptor also binds several other lipoxygenase-products, such as 12S-HETE, 12S-HPETE, 15S-HETE, and the thromboxane synthase product 12-hydroxyheptadecatrienoic acid. The BLT receptors mediate chemotaxis and immunomodulation in several leukocyte populations and are in addition expressed on non-myeloid cells, such as vascular smooth muscle and endothelial cells. In addition to BLT receptors, LTB4 has been reported to bind to the peroxisome proliferator activated receptor (PPAR) α [196] and the vanilloid TRPV1 ligand-gated nonselective cation channel [217]. The receptors for the cysteinyl-leukotrienes (i.e. LTC4, LTD4 and LTE4) are termed CysLT1 and CysLT2 and exhibit distinct expression patterns in human tissues, mediating for example smooth muscle cell contraction, regulation of vascular permeability, and leukocyte activation. There is also evidence in the literature for additional CysLT receptor subtypes, derived from functional in vitro studies, radioligand binding and in mice lacking both CysLT1 and CysLT2 receptors [37]. Cysteinyl-leukotrienes have also been suggested to signal through the P2Y12 receptor [96, 243, 272], GPR17 [57] and GPR99 [168].

ACS Style

Magnus Bäck; Charles Brink; Nan Chiang; Sven-Erik Dahlén; Gordon Dent; Jeffrey Drazen; Jilly F. Evans; Douglas W. P. Hay; Motonao Nakamura; William Powell; Joshua Rokach; G. Enrico Rovati; Charles N. Serhan; Takao Shimizu; Mohib Uddin; Takehiko Yokomizo. Leukotriene receptors (version 2020.3) in the IUPHAR/BPS Guide to Pharmacology Database. IUPHAR/BPS Guide to Pharmacology CITE 2020, 2020, 1 .

AMA Style

Magnus Bäck, Charles Brink, Nan Chiang, Sven-Erik Dahlén, Gordon Dent, Jeffrey Drazen, Jilly F. Evans, Douglas W. P. Hay, Motonao Nakamura, William Powell, Joshua Rokach, G. Enrico Rovati, Charles N. Serhan, Takao Shimizu, Mohib Uddin, Takehiko Yokomizo. Leukotriene receptors (version 2020.3) in the IUPHAR/BPS Guide to Pharmacology Database. IUPHAR/BPS Guide to Pharmacology CITE. 2020; 2020 (3):1.

Chicago/Turabian Style

Magnus Bäck; Charles Brink; Nan Chiang; Sven-Erik Dahlén; Gordon Dent; Jeffrey Drazen; Jilly F. Evans; Douglas W. P. Hay; Motonao Nakamura; William Powell; Joshua Rokach; G. Enrico Rovati; Charles N. Serhan; Takao Shimizu; Mohib Uddin; Takehiko Yokomizo. 2020. "Leukotriene receptors (version 2020.3) in the IUPHAR/BPS Guide to Pharmacology Database." IUPHAR/BPS Guide to Pharmacology CITE 2020, no. 3: 1.

Research article
Published: 01 June 2020 in Circulation: Genomic and Precision Medicine
Reads 0
Downloads 0

Background: Aortic stenosis (AS) contributes to cardiovascular mortality and morbidity but disease mechanisms remain largely unknown. Recent evidence associates a single nucleotide polymorphism rs174547 within the FADS1 gene, encoding FADS1 (fatty acid desaturase 1), with risk of several cardiovascular outcomes, including AS. FADS1 encodes a rate-limiting enzyme for ω-3 and ω-6 fatty acid metabolism. The aim of this study was to decipher the local transcriptomic and lipidomic consequences of rs174547 in tricuspid aortic valves from patients with AS. Methods: Expression quantitative trait loci study was performed using data from Illumina Human610-Quad BeadChip, Infinium Global Screening Arrays, and Affymetrix Human Transcriptome 2.0 arrays in calcified and noncalcified aortic valve tissue from 58 patients with AS (mean age, 74.2; SD, 5.9). Fatty acid content was assessed in aortic valves from 25 patients with AS using gas chromatography. Δ 5 and Δ 6 desaturase activity was assessed by the product-to-precursor ratio. Results: The minor C-allele of rs174547, corresponding to the protective genotype for AS, was associated with higher FADS2 mRNA levels in calcified valve tissue, whereas FADS1 mRNA and other transcripts in proximity of the single nucleotide polymorphism were unaltered. In contrast, the FADS1 Δ 5-desaturase activity and the FADS2 Δ 6-desaturase activity were decreased. Finally, docosahexaenoic acid was decreased in calcified tissue compared with non-calcified tissue and C-allele carriers exhibited increased docosahexaenoic acid levels. Overall desaturase activity measured with ω-3 fatty acids was higher in C-allele carriers. Conclusions: The association between the FADS1 genotype and AS may implicate effects on valvular fatty acids.

ACS Style

Oscar Plunde; Susanna C. Larsson; Gonzalo Artiach; George Thanassoulis; Miguel Carracedo; Anders Franco-Cereceda; Per Eriksson; Magnus Bäck. FADS1 (Fatty Acid Desaturase 1) Genotype Associates With Aortic Valve FADS mRNA Expression, Fatty Acid Content and Calcification. Circulation: Genomic and Precision Medicine 2020, 13, e002710 -e002710.

AMA Style

Oscar Plunde, Susanna C. Larsson, Gonzalo Artiach, George Thanassoulis, Miguel Carracedo, Anders Franco-Cereceda, Per Eriksson, Magnus Bäck. FADS1 (Fatty Acid Desaturase 1) Genotype Associates With Aortic Valve FADS mRNA Expression, Fatty Acid Content and Calcification. Circulation: Genomic and Precision Medicine. 2020; 13 (3):e002710-e002710.

Chicago/Turabian Style

Oscar Plunde; Susanna C. Larsson; Gonzalo Artiach; George Thanassoulis; Miguel Carracedo; Anders Franco-Cereceda; Per Eriksson; Magnus Bäck. 2020. "FADS1 (Fatty Acid Desaturase 1) Genotype Associates With Aortic Valve FADS mRNA Expression, Fatty Acid Content and Calcification." Circulation: Genomic and Precision Medicine 13, no. 3: e002710-e002710.

Review
Published: 04 April 2020 in Toxins
Reads 0
Downloads 0

Persistent low-grade inflammation and premature ageing are hallmarks of the uremic phenotype and contribute to impaired health status, reduced quality of life, and premature mortality in chronic kidney disease (CKD). Because there is a huge global burden of disease due to CKD, treatment strategies targeting inflammation and premature ageing in CKD are of particular interest. Several distinct features of the uremic phenotype may represent potential treatment options to attenuate the risk of progression and poor outcome in CKD. The nuclear factor erythroid 2-related factor 2 (NRF2)–kelch-like erythroid cell-derived protein with CNC homology [ECH]-associated protein 1 (KEAP1) signaling pathway, the endocrine phosphate-fibroblast growth factor-23–klotho axis, increased cellular senescence, and impaired mitochondrial biogenesis are currently the most promising candidates, and different pharmaceutical compounds are already under evaluation. If studies in humans show beneficial effects, carefully phenotyped patients with CKD can benefit from them.

ACS Style

Thomas Ebert; Sven-Christian Pawelzik; Anna Witasp; Samsul Arefin; Sam Hobson; Karolina Kublickiene; Paul G. Shiels; Magnus Bäck; Peter Stenvinkel. Inflammation and Premature Ageing in Chronic Kidney Disease. Toxins 2020, 12, 227 .

AMA Style

Thomas Ebert, Sven-Christian Pawelzik, Anna Witasp, Samsul Arefin, Sam Hobson, Karolina Kublickiene, Paul G. Shiels, Magnus Bäck, Peter Stenvinkel. Inflammation and Premature Ageing in Chronic Kidney Disease. Toxins. 2020; 12 (4):227.

Chicago/Turabian Style

Thomas Ebert; Sven-Christian Pawelzik; Anna Witasp; Samsul Arefin; Sam Hobson; Karolina Kublickiene; Paul G. Shiels; Magnus Bäck; Peter Stenvinkel. 2020. "Inflammation and Premature Ageing in Chronic Kidney Disease." Toxins 12, no. 4: 227.

Journal article
Published: 17 March 2020 in JACC: CardioOncology
Reads 0
Downloads 0
ACS Style

Miguel Carracedo; Leif Stenke; Anders Franco-Cereceda; Magnus Bäck. Aortic Stenosis and the Tyrosine Kinase Inhibitor Nilotinib in Chronic Myeloid Leukemia. JACC: CardioOncology 2020, 2, 123 -126.

AMA Style

Miguel Carracedo, Leif Stenke, Anders Franco-Cereceda, Magnus Bäck. Aortic Stenosis and the Tyrosine Kinase Inhibitor Nilotinib in Chronic Myeloid Leukemia. JACC: CardioOncology. 2020; 2 (1):123-126.

Chicago/Turabian Style

Miguel Carracedo; Leif Stenke; Anders Franco-Cereceda; Magnus Bäck. 2020. "Aortic Stenosis and the Tyrosine Kinase Inhibitor Nilotinib in Chronic Myeloid Leukemia." JACC: CardioOncology 2, no. 1: 123-126.

Journal article
Published: 11 March 2020 in Cells
Reads 0
Downloads 0

Aortic valve stenosis (AVS), a consequence of increased fibrosis and calcification of the aortic valve leaflets, causes progressive narrowing of the aortic valve. Proteoglycans, structural components of the aortic valve, accumulate in regions with fibrosis and moderate calcification. Particularly, proteoglycan 4 (PRG4) has been identified in fibrotic parts of aortic valves. However, the role of PRG4 in the context of AVS and aortic valve calcification has not yet been determined. Here, transcriptomics, histology, and immunohistochemistry were performed in human aortic valves from patients undergoing aortic valve replacement. Human valve interstitial cells (VICs) were used for calcification experiments and RNA expression analysis. PRG4 was significantly upregulated in thickened and calcified regions of aortic valves compared with healthy regions. In addition, mRNA levels of PRG4 positively associated with mRNA for proteins involved in cardiovascular calcification. Treatment of VICs with recombinant human PRG4 enhanced phosphate-induced calcification and increased the mRNA expression of bone morphogenetic protein 2 and the runt-related transcription factor 2. In summary, PRG4 was upregulated in the development of AVS and promoted VIC osteogenic differentiation and calcification. These results suggest that an altered valve leaflet proteoglycan composition may play a role in the progression of AVS.

ACS Style

Gonzalo Artiach; Miguel Carracedo; Till Seime; Oscar Plunde; Andres Laguna-Fernandez; Ljubica Matic; Anders Franco-Cereceda; Magnus Bäck. Proteoglycan 4 is Increased in Human Calcified Aortic Valves and Enhances Valvular Interstitial Cell Calcification. Cells 2020, 9, 684 .

AMA Style

Gonzalo Artiach, Miguel Carracedo, Till Seime, Oscar Plunde, Andres Laguna-Fernandez, Ljubica Matic, Anders Franco-Cereceda, Magnus Bäck. Proteoglycan 4 is Increased in Human Calcified Aortic Valves and Enhances Valvular Interstitial Cell Calcification. Cells. 2020; 9 (3):684.

Chicago/Turabian Style

Gonzalo Artiach; Miguel Carracedo; Till Seime; Oscar Plunde; Andres Laguna-Fernandez; Ljubica Matic; Anders Franco-Cereceda; Magnus Bäck. 2020. "Proteoglycan 4 is Increased in Human Calcified Aortic Valves and Enhances Valvular Interstitial Cell Calcification." Cells 9, no. 3: 684.

Comment
Published: 25 February 2020 in Kardiologia Polska
Reads 0
Downloads 0
ACS Style

Gonzalo Artiach; Philip Sarajlic; Magnus Bäck. Inflammation and its resolution in coronary artery disease: a tightrope walk between omega-6 and omega-3 polyunsaturated fatty acids. Kardiologia Polska 2020, 78, 93 -95.

AMA Style

Gonzalo Artiach, Philip Sarajlic, Magnus Bäck. Inflammation and its resolution in coronary artery disease: a tightrope walk between omega-6 and omega-3 polyunsaturated fatty acids. Kardiologia Polska. 2020; 78 (2):93-95.

Chicago/Turabian Style

Gonzalo Artiach; Philip Sarajlic; Magnus Bäck. 2020. "Inflammation and its resolution in coronary artery disease: a tightrope walk between omega-6 and omega-3 polyunsaturated fatty acids." Kardiologia Polska 78, no. 2: 93-95.

Journal article
Published: 24 February 2020 in Journal of Clinical Medicine
Reads 0
Downloads 0

Background: Aortic valve calcium (AVC) and coronary artery calcium (CAC) are common complications in end-stage renal disease (ESRD). We investigated the prognostic significance of overlapping presence of AVC and CAC, and whether AVC was associated with all-cause mortality independent of the presence of CAC in ESRD. Methods: 259 ESRD patients (median age 55 years, 67% males) undergoing cardiac computed tomography were included. Framingham risk score (FRS), presence of cardiovascular disease (CVD), statin use, nutritional status and other relevant laboratory data were determined at baseline. During follow-up for median 36 months, 44 patients died, and 68 patients underwent renal transplantation. Results: The baseline overlap presence of AVC and CAC was 37%. Multivariate regression analysis showed that FRS (odds ratio (OR) 2.25; 95% confidence interval (95% CI), 1.43–3.55) and CAC score (OR (95% CI), 2.18 (1.34–3.59)) were independent determinants of AVC. In competing-risk regression models adjusted for presence of CAC, inflammation, nutritional status, CVD, FRS and statin use, AVC remained independently associated with all-cause mortality (sub-hazard ratio (95% CI), 2.57 (1.20–5.51)). Conclusions: The overlap of AVC and CAC was 37% in this ESRD cohort. AVC was associated with increased all-cause mortality independent of presence of CAC, traditional risk factors and inflammation.

ACS Style

Lu Dai; Oscar Plunde; Abdul Rashid Qureshi; Bengt Lindholm; Torkel B. Brismar; Leon J. Schurgers; Magnus Söderberg; Jonaz Ripsweden; Magnus Bäck; Peter Stenvinkel. Aortic Valve Calcium Associates with All-Cause Mortality Independent of Coronary Artery Calcium and Inflammation in Patients with End-Stage Renal Disease. Journal of Clinical Medicine 2020, 9, 607 .

AMA Style

Lu Dai, Oscar Plunde, Abdul Rashid Qureshi, Bengt Lindholm, Torkel B. Brismar, Leon J. Schurgers, Magnus Söderberg, Jonaz Ripsweden, Magnus Bäck, Peter Stenvinkel. Aortic Valve Calcium Associates with All-Cause Mortality Independent of Coronary Artery Calcium and Inflammation in Patients with End-Stage Renal Disease. Journal of Clinical Medicine. 2020; 9 (2):607.

Chicago/Turabian Style

Lu Dai; Oscar Plunde; Abdul Rashid Qureshi; Bengt Lindholm; Torkel B. Brismar; Leon J. Schurgers; Magnus Söderberg; Jonaz Ripsweden; Magnus Bäck; Peter Stenvinkel. 2020. "Aortic Valve Calcium Associates with All-Cause Mortality Independent of Coronary Artery Calcium and Inflammation in Patients with End-Stage Renal Disease." Journal of Clinical Medicine 9, no. 2: 607.

Research article
Published: 14 January 2020 in Oxidative Medicine and Cellular Longevity
Reads 0
Downloads 0

Introduction. Calcific aortic valve stenosis (CAVS) is a common disease associated with aging. Oxidative stress participates in the valve calcification process in CAVS. Semicarbazide-sensitive amine oxidase (SSAO), also referred to as vascular adhesion protein 1 (VAP-1), transforms primary amines into aldehydes, generating hydrogen peroxide and ammonia. SSAO is expressed in calcified aortic valves, but its role in valve calcification has remained largely unexplored. The aims of this study were to characterize the expression and the activity of SSAO during aortic valve calcification and to establish the effects of SSAO inhibition on human valvular interstitial cell (VIC) calcification. Methods. Human aortic valves from n=80 patients were used for mRNA extraction and expression analysis, Western blot, SSAO activity determination, immunohistochemistry, and the isolation of primary VIC cultures. Results. SSAO mRNA, protein, and activity were increased with increasing calcification within human aortic valves and localized in the vicinity of the calcified zones. The valvular SSAO upregulation was consistent after stratification of the subjects according to cardiovascular and CAVS risk factors associated with increased oxidative stress: body mass index, diabetes, and smoking. SSAO mRNA levels were significantly associated with poly(ADP-ribose) polymerase 1 (PARP1) in calcified tissue. Calcification of VIC was inhibited in the presence of the specific SSAO inhibitor LJP1586. Conclusion. The association of SSAO expression and activity with valvular calcification and oxidative stress as well as the decreased VIC calcification by SSAO inhibition points to SSAO as a possible marker and therapeutic target to be further explored in CAVS.

ACS Style

Nathalie Mercier; Sven-Christian Pawelzik; John Pirault; Miguel Carracedo; Oscar Persson; Bastien Wollensack; Anders Franco-Cereceda; Magnus Bäck. Semicarbazide-Sensitive Amine Oxidase Increases in Calcific Aortic Valve Stenosis and Contributes to Valvular Interstitial Cell Calcification. Oxidative Medicine and Cellular Longevity 2020, 2020, 1 -9.

AMA Style

Nathalie Mercier, Sven-Christian Pawelzik, John Pirault, Miguel Carracedo, Oscar Persson, Bastien Wollensack, Anders Franco-Cereceda, Magnus Bäck. Semicarbazide-Sensitive Amine Oxidase Increases in Calcific Aortic Valve Stenosis and Contributes to Valvular Interstitial Cell Calcification. Oxidative Medicine and Cellular Longevity. 2020; 2020 ():1-9.

Chicago/Turabian Style

Nathalie Mercier; Sven-Christian Pawelzik; John Pirault; Miguel Carracedo; Oscar Persson; Bastien Wollensack; Anders Franco-Cereceda; Magnus Bäck. 2020. "Semicarbazide-Sensitive Amine Oxidase Increases in Calcific Aortic Valve Stenosis and Contributes to Valvular Interstitial Cell Calcification." Oxidative Medicine and Cellular Longevity 2020, no. : 1-9.