Christensen group: Cellular and molecular biology of myocardial hypertrophy

We aim to develop novel therapeutic approaches and better diagnostic tools for heart failure through new knowledge about molecular mechanisms involved.

 

 

In particular, we study the concept that cardiac proteoglycans are active and central signal mediators of myocardial remodeling. Proteoglycans are highly glycosylated proteins localized to the cell membranes and the extracellular matrix (ECM).

By examining the unique properties of transmembrane proteoglycans we have discovered that the proteoglycan syndecan-4 is a mechanical stress-sensor in cardiomyocytes and cardiac fibroblasts and involved in signalling causing heart failure. One important ECM-localized molecule is lumican and we have shown that it regulates cardiac remodelling and heart failure. Currently we are testing promising drugs to treat heart failure by targeting mechanisms identified by our group. The ultimate goal of our research is to improve the well-being and prognosis of patients.

 

The work in this group is supervised by professor Geir Christensen. The group consists of scientists from IEMR that collaborate closely with Department of Thoracic Surgery (Professor Theis Tønnessen) and Department of Cardiology at Oslo University Hospital (Professor Lars Gullestad). In addition to top-of-the-range international scientists from Harvard, Johns Hopkins, among others, who are world leading in their field.

Group Leader

Geir Christensen

Group Leader & Professor

Group members

Andreas Romaine

Postdoctoral fellow

Athiramol Sasi

Doctoral Research Fellow

Chloe Rixon

Doctoral Research Fellow

Maria Vistnes

Postdoctoral fellow, Resident

Associated members

Camilla Udjus

Doctoral Research Fellow

Francesca Lockwood

Doctoral Research Fellow

Latest publications

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Vistnes M, Erusappan PM, Sasi A, Nordén ES, Bergo K, Romaine A, Lunde IG, Zhang L, Olsen MB, Øgaard J, Carlson CR, Wang CH, Riise J, Dahl CP, Fiane AE, Hauge-Iversen I, Espe E, Melleby AO, Tønnessen T, Aronsen JM, Sjaastad I, Christensen G (2023)
Inhibition of the extracellular enzyme ADAMTS4 prevents cardiac fibrosis and dysfunction
Cardiovasc Res
PubMed 37216909 DOI 10.1093/cvr/cvad078
Perdreau-Dahl H, Lipsett DB, Frisk M, Kermani F, Carlson CR, Brech A, Shen X, Bergan-Dahl A, Hou Y, Tuomainen T, Tavi P, Jones PP, Lunde M, Wasserstrom JA, Laporte J, Ullrich ND, Christensen G, Morth JP, Louch WE (2023)
BIN1, Myotubularin, and Dynamin-2 Coordinate T-Tubule Growth in Cardiomyocytes
Circ Res, 132 (11), e188-e205
PubMed 37139790 DOI 10.1161/CIRCRESAHA.122.321732
Andreassen K, Rixon C, Hansen MH, Hauge-Iversen IM, Zhang L, Sadredini M, Erusappan PM, Sjaastad I, Christensen G, Haugaa KH, Edvardsen T, Lunde IG, Stokke MK (2023)
Beneficial effects of exercise initiated before development of hypertrophic cardiomyopathy in genotype-positive mice
Am J Physiol Heart Circ Physiol, 324 (6), H881-H892
PubMed 37115627 DOI 10.1152/ajpheart.00701.2022
Strand ME, Vanhaverbeke M, Henkens MTHM, Sikking MA, Rypdal KB, Braathen B, Almaas VM, Tønnessen T, Christensen G, Heymans S, Lunde IG (2023)
Inflammation and Syndecan-4 Shedding from Cardiac Cells in Ischemic and Non-Ischemic Heart Disease
Biomedicines, 11 (4)
PubMed 37189684 DOI 10.3390/biomedicines11041066
Rypdal KB, Olav Melleby A, Robinson EL, Li J, Palmero S, Seifert DE, Martin D, Clark C, López B, Andreassen K, Dahl CP, Sjaastad I, Tønnessen T, Stokke MK, Louch WE, González A, Heymans S, Christensen G, Apte SS, Lunde IG (2022)
ADAMTSL3 knock-out mice develop cardiac dysfunction and dilatation with increased TGFβ signalling after pressure overload
Commun Biol, 5 (1), 1392
PubMed 36539599 DOI 10.1038/s42003-022-04361-1
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