Christensen group: Cellular and molecular biology of myocardial hypertrophy

Christensen group

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

Camilla Udjus

Doctoral Research Fellow

Chloe Rixon

Doctoral Research Fellow

Francesca Lockwood

Doctoral Research Fellow

Maria Vistnes

Postdoctoral fellow, Resident

Latest publications

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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
Rixon C, Andreassen K, Shen X, Erusappan PM, Almaas VM, Palmero S, Dahl CP, Ueland T, Sjaastad I, Louch WE, Stokke MK, Tønnessen T, Christensen G, Lunde IG (2022)
Lumican accumulates with fibrillar collagen in fibrosis in hypertrophic cardiomyopathy
ESC Heart Fail
PubMed 36444917 DOI 10.1002/ehf2.14234
Lunde IG, Aronsen JM, Melleby AO, Strand ME, Skogestad J, Bendiksen BA, Ahmed MS, Sjaastad I, Attramadal H, Carlson CR, Christensen G (2022)
Cardiomyocyte-specific overexpression of syndecan-4 in mice results in activation of calcineurin-NFAT signalling and exacerbated cardiac hypertrophy
Mol Biol Rep, 49 (12), 11795-11809
PubMed 36205855 DOI 10.1007/s11033-022-07985-y
Støle TP, Lunde M, Shen X, Martinsen M, Lunde PK, Li J, Lockwood F, Sjaastad I, Louch WE, Aronsen JM, Christensen G, Carlson CR (2022)
The female syndecan-4-/- heart has smaller cardiomyocytes, augmented insulin/pSer473-Akt/pSer9-GSK-3β signaling, and lowered SCOP, pThr308-Akt/Akt and GLUT4 levels
Front Cell Dev Biol, 10, 908126
PubMed 36092718 DOI 10.3389/fcell.2022.908126
Andreassen K, Dejgaard LA, Lie Ø, Fink TS, Lunde IG, Edvardsen T, Haugaa KH, Stokke MK (2022)
Exercise training during childhood and adolescence is associated with favorable diastolic function in hypertrophic cardiomyopathy
Int J Cardiol, 364, 65-71
PubMed 35714718 DOI 10.1016/j.ijcard.2022.06.042
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