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Inflammation in heart failure

We study the role of inflammation in the development of cardiovascular disease. We have a translation research approach, and combine studies of clinical material with experimental in vivo and in vitro models.

About the group

Cardiovascular disease (CVD) is the leading cause of death globally. Most forms of CVD are associated with inflammation. Atherosclerosis and chronic heart failure are conditions characterized by a chronic non-resolving inflammatory phenotype, while myocardial infarction and stroke, the direct consequences of atherosclerosis, are acute inflammatory conditions. Our main hypothesis is that these inflammatory processes, chronic or acute, directly contribute to the pathogenesis of CVD. During the recent years our group has gradually shift the focus from heart failure to atherosclerosis and obesity and related metabolic disturbances.

By studying how specific components of the inflammatory response affects CVD progression and also how inflammation is initiated, maintained and terminated, our group has the ambitious aim to develop novel strategies for preventing, identifying and treating different forms of CVD and related metabolic disorders. 

Our group has a translational research profile. We use experimental mouse models to mimic CVD development and characterize the pathogenic processes involved. In addition, our research approach includes in vitro studies in primary isolated cells from man and mouse, as well as clinical studies in well characterized patients with CVD, examining samples from peripheral blood as well as tissue samples. The ultimate goal is to develop new treatment modalities in CVD and related disorders.

The group belongs to the Department of Internal Medicine


  • Role of NLRP3 inflammasome in cardiac injury and stress.
  • Inflammaging – The interaction between aging and inflammation in cardiovascular disease.
  • Metaflammation – The interaction between metabolical function and inflammation in cardiovascular disease.
  • Role of the DNA glycosylase Neil3 in cardiac disease.
  • Interaction between DNA damage, mitochondrial function and inflammation in cardiovascular disease.
  • Role of complement and toll-like receptor signaling in development of heart failure.
  • Mechanisms for resolution of inflammation – Therapeutic potential in cardiac disease



  • Prof. Pål Aukrust, Institutt for Indremedisinsk forskning, KIT, OUS
  • Prof. Bente Halvorsen, Institutt for Indremedisinsk forskning, KIT, OUS
  • Prof. Thor Ueland, Institutt for Indremedisinsk forskning, KIT, OUS
  • Prof. Tom Eirik Mollnes, Avd. for Immunologi, OUS
  • Prof. Lars Gullestad, Kardiologisk avdeling, OUS Rikshospitalet
  • Dr. Geir Øystein Andersen, Kardiologisk avdeling, OUS Ullevål


  • Prof. Magnar Bjørås, Avd. kreftforskning og molekylærmedisin, NTNU
  • Prof. Ivar Sjaastad, Institutt for eksperimentell medisinsk forskning, OUS Ullevål
  • Prof. Kåre-Olav Stensløkken, Institutt for Medisinske basalfag, UiO


  • Prof. Erik A. Biessen, University of Maastricht, The Netherlands

Selected Publications

Complement component C3 and the TLR co-receptor CD14 are not involved in angiotensin II induced cardiac remodelling.
Shahini N, Schjalm C, Nilsson PH, Holt MF, Øgaard JDS, Lien E, Ahmed MS, Attramadal H, Aukrust P, Yndestad A, Mollnes TE, Louwe MC.
Biochem Biophys Res Commun. 2020 Mar 19;523(4):867-873. doi: 10.1016/j.bbrc.2020.01.018. Epub 2020 Jan 16.

Selective and marked decrease of complement receptor C5aR2 in human thoracic aortic aneurysms: a dysregulation with potential inflammatory effects.
Holt M, Seim BE, Øgaard J, Olsen MB, Woldbæk PR, Kvitting JP, Aukrust P, Yndestad A, Mollnes TE, Nilsson PH, Louwe MC, Ranheim T.
Open Heart. 2019 Nov 10;6(2):e001098. doi: 10.1136/openhrt-2019-001098. eCollection 2019.
NLRP3 Inflammasome: A Novel Player in Metabolically Induced Inflammation-Potential Influence on the Myocardium.
Sokolova M, Ranheim T, Louwe MC, Halvorsen B, Yndestad A, Aukrust P.
J Cardiovasc Pharmacol. 2019 Oct;74(4):276-284. doi: 10.1097/FJC.0000000000000704.

Low Cellular NAD+ Compromises Lipopolysaccharide-Induced Inflammatory Responses via Inhibiting TLR4 Signal Transduction in Human Monocytes.
Yang K, Lauritzen KH, Olsen MB, Dahl TB, Ranheim T, Ahmed MS, Attramadal H, Aukrust P, Halvorsen B, Nyman TA, Sandanger Ø, Yndestad A.
J Immunol. 2019 Sep 15;203(6):1598-1608. doi: 10.4049/jimmunol.1801382. Epub 2019 Aug 19.

NLRP3 Inflammasome Promotes Myocardial Remodeling During Diet-Induced Obesity.
Sokolova M, Sjaastad I, Louwe MC, Alfsnes K, Aronsen JM, Zhang L, Haugstad SB, Bendiksen BA, Øgaard J, Bliksøen M, Lien E, Berge RK, Aukrust P, Ranheim T, Yndestad A.
Front Immunol. 2019 Jul 16;10:1621. doi: 10.3389/fimmu.2019.01621. eCollection 2019.

NLRP3 inflammasome: a novel player in metabolically-induced inflammation - potential influence on the myocardium.
Sokolova M, Ranheim T, Louwe MC, Halvorsen B, Yndestad A, Aukrust P.
J Cardiovasc Pharmacol. 2019 Jul 22. doi: 10.1097/FJC.0000000000000704. [Epub ahead of print]

Early increase of specialized pro-resolving lipid mediators in patients with ST-elevation myocardial infarction.
Fosshaug LE, Colas RA, Anstensrud AK, Gregersen I, Nymo S, Sagen EL, Michelsen A, Vinge LE, Øie E, Gullestad L, Halvorsen B, Hansen TV, Aukrust P, Dalli J, Yndestad A.
EBioMedicine. 2019 Aug;46:264-273. doi: 10.1016/j.ebiom.2019.07.024. Epub 2019 Jul 22.
Mammalian Target of Rapamycin (mTOR) and the Proteasome Attenuates IL-1β Expression in Primary Mouse Cardiac Fibroblasts.
Torp MK, Yang K, Ranheim T, Husø Lauritzen K, Alfsnes K, Vinge LE, Aukrust P, Stensløkken KO, Yndestad A, Sandanger Ø.
Front Immunol. 2019 Jun 6;10:1285. doi: 10.3389/fimmu.2019.01285. eCollection 2019.

NLRP3 inflammasome mediates oxidative stress-induced pancreatic islet dysfunction.
Sokolova M, Sahraoui A, Høyem M, Øgaard J, Lien E, Aukrust P, Yndestad A, Ranheim T, Scholz H.
Am J Physiol Endocrinol Metab. 2018 Nov 1;315(5):E912-E923. doi: 10.1152/ajpendo.00461.2017. Epub 2018 Jul 17.

Leukocyte Overexpression of Intracellular NAMPT Attenuates Atherosclerosis by Regulating PPARγ-Dependent Monocyte Differentiation and Function.
Bermudez B, Dahl TB, Medina I, Groeneweg M, Holm S, Montserrat-de la Paz S, Rousch M, Otten J, Herias V, Varela LM, Ranheim T, Yndestad A, Ortega-Gomez A, Abia R, Nagy L, Aukrust P, Muriana FJG, Halvorsen B, Biessen EAL.
Arterioscler Thromb Vasc Biol. 2017 Jun;37(6):1157-1167. doi: 10.1161/ATVBAHA.116.308187. Epub 2017 Apr 13.

Toll-Like Receptor 9 Promotes Survival in SERCA2a KO Heart Failure Mice.
Dhondup Y, Sjaastad I, Sandanger Ø, Aronsen JM, Ahmed MS, Attramadal H, Finsen AV, Zhang L, Ranheim T, Alfsnes K, Aukrust P, Christensen G, Yndestad A, Vinge LE.
Mediators Inflamm. 2017;2017:9450439. doi: 10.1155/2017/9450439. Epub 2017 Apr 11.
NEIL3-Dependent Regulation of Cardiac Fibroblast Proliferation Prevents Myocardial Rupture.
Olsen MB, Hildrestrand GA, Scheffler K, Vinge LE, Alfsnes K, Palibrk V, Wang J, Neurauter CG, Luna L, Johansen J, Øgaard JDS, Ohm IK, Slupphaug G, Kuśnierczyk A, Fiane AE, Brorson SH, Zhang L, Gullestad L, Louch WE, Iversen PO, Østlie I, Klungland A, Christensen G, Sjaastad I, Sætrom P, Yndestad A, Aukrust P, Bjørås M, Finsen AV.
Cell Rep. 2017 Jan 3;18(1):82-92. doi: 10.1016/j.celrep.2016.12.009.



Published Aug. 10, 2018 10:24 AM - Last modified Apr. 28, 2021 2:55 PM


Group leader


  • Trine Ranheim
  • Pål Aukrust
  • Azita Rashidi
  • Jonas Øgaard
  • Knut Husø Lauritzen
  • Kuan Yang
  • Margrethe F. Holt.
  • Maria Belland Olsen
  • Mieke Louwe
  • Øystein Sandanger
Detailed list of participants