CERIC Center of Excellence for Research on Inflammation and Cardiovascular disease

Magnus Bäck | Featured Publications

ERV1/ChemR23 Signaling Protects from Atherosclerosis by Modifying oxLDL Uptake and Phagocytosis in Macrophages

Andres Laguna-Fernandez, Antonio Checa, Miguel Carracedo, Gonzalo Artiach, Marcelo H. Petri, Roland Baumgartner, Maria J. Forteza, Xintong Jiang, Teodora Andonova, Mary E. Walker, Jesmond Dalli, Hildur Arnardottir, Anton Gisterå, Silke Thul, Craig E. Wheelock, Gabrielle Paulsson-Berne, Daniel F. J. Ketelhuth, Göran K. Hansson, Magnus Bäck. Circulation. 2018, 2018 May 8. doi: 10.1161/CIRCULATIONAHA.117.032801
In addition to enhanced pro-inflammatory signaling, impaired resolution of vascular inflammation plays a key role in atherosclerosis. Pro-resolving lipid mediators formed through the 12/15 lipoxygenase pathways exert protective effects against murine atherosclerosis. n-3 polyunsaturated fatty acids, including eicosapentaenoic acid (EPA), serve as the substrate for the formation of lipid mediators, which transduce potent anti-inflammatory and pro-resolving actions through their cognate G-protein-coupled receptors. The aim of this study was to identify signaling pathways associated with EPA supplementation and lipid mediator formation that mediate atherosclerotic disease progression.

Aspirin-triggered 15-epi-lipoxin A4 signals through FPR2/ALX in vascular smooth muscle cells and protects against intimal hyperplasia after carotid ligation

Marcelo H. Petri, Andrés Laguna-Fernandez, Chi-Nan Tseng, Ulf Hedin, Mauro Perretti, Magnus Bäck. International Journal of Cardiology. 2015, (179)370–372.
The benefit of aspirin is well established in cardiovascular prevention, and involves the irreversible inhibition of platelet cyclooxygenase (COX)-1 and, as a consequence, decreased thromboxane levels [1]. In addition to inhibition of platelet aggregation, aspirin may also have anti-inflammatory properties, with potential additional benefit in atherosclerosis prevention. Acetylation of the COX-2 enzyme by aspirin directs the metabolism of polyunsaturated fatty acids (PUFAs) towards a biosynthetic pathway, which in addition involves lipoxygenase enzymes and leads to the formation of specific mediators, such as 15-epi-lipoxin A4, also referred to as aspirin-triggered lipoxin (ATL) [2].

Leukotrienes as a molecular link between obstructive sleep apnoea and atherosclerosis

Françoise Stanke-Labesque, Jean-Louis Pépin, Elodie Gautier-Veyret, Patrick Lévy and Magnus Bäck. Cardiovascular Research [Epub ahead of print] (2013).
Leukotrienes are biologically active lipid mediators of inflammation involved in atherogenesis. Obstructive sleep apnoea (OSA) patients exhibit early atherosclerosis and activation of the leukotriene pathway. In OSA patients, the production of leukotrienes is increased in relation to OSA severity and in vitro exposure of immune cells to intermittent hypoxia increases leukotriene pathway transcription. Moreover, the leukotriene transcriptional pathway is associated with early vascular remodelling. Lastly, obesity is a major confounding factor for leukotriene activation in OSA. The aim of this review was to focus on the intricate network of leukotrienes, chronic intermittent hypoxia, and atherosclerosis, with an emphasis on the role of leukotrienes in the early atherosclerosis observed in OSA patients.