Cardiomyocyte function in health and disease

Louch group

Our research is aimed at understanding abnormal cellular calcium handling, with focus on the structures and proteins that control calcium cycling.

Cardiac function is tightly controlled by the contraction and relaxation of these cells; processes which are in turn reliant on carefully controlled calcium homeostasis. Indeed, cardiac dysfunction during diseases such as heart failure and atrial fibrillation can often be traced to abnormal cellular calcium handling.

Our research is aimed at understanding these abnormalities, with focus on the structures and proteins that control calcium cycling. How are these structures and proteins put together during development, and what causes them to disassemble during disease? What is the consequence of such alterations? To examine these questions, we combine molecular biology and electrophysiology techniques with advanced 3D imaging (super-resolution, confocal, and electron microscopy).

Ultimately, we strive to mechanistically link subcellular structure and calcium handling to whole-heart function, and to reverse dysfunction during disease for the benefit of patients.

Group leader William (Bill) Louch is a Professor of Medicine and Head of the Core Facility for Advanced Light Microscopy. He currently holds a Consolidator Grant from the European Research Council which was initiated in 2015. His group’s research is focused on understanding the structure and function cardiac muscle cells.

Group members

Anna Bergan Dahl

Doctoral Research Fellow

Christopher Le

Researcher without PhD

Harmonie Perdreau-Dahl

Postdoctoral fellow

Jia Li

Postdoctoral fellow

Martin Laasmaa

Postdoctoral fellow

Ornella Manfra

Postdoctoral fellow

Terje Kolstad

Researcher without PhD

Victoria Becker

Doctoral Research Fellow

Xin Shen

Postdoctoral fellow

Yufeng Hou

Postdoctoral fellow

Latest publications

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Kobirumaki-Shimozawa F, Shimozawa T, Oyama K, Baba S, Li J, Nakanishi T, Terui T, Louch WE, Ishiwata S, Fukuda N (2021)
Synchrony of sarcomeric movement regulates left ventricular pump function in the in vivo beating mouse heart
J Gen Physiol, 153 (11)
PubMed 34605861 DOI 10.1085/jgp.202012860
Setterberg IE, Le C, Frisk M, Li J, Louch WE (2021)
The Physiology and Pathophysiology of T-Tubules in the Heart
Front Physiol, 12, 718404
PubMed 34566684 DOI 10.3389/fphys.2021.718404
Rohner E, Witman N, Sohlmer J, De Genst E, Louch WE, Sahara M, Chien KR (2021)
An mRNA assay system demonstrates proteasomal-specific degradation contributes to cardiomyopathic phospholamban null mutation
Mol Med, 27 (1), 102
PubMed 34496741 DOI 10.1186/s10020-021-00362-8
Grote Beverborg N, Später D, Knöll R, Hidalgo A, Yeh ST, Elbeck Z, Silljé HHW, Eijgenraam TR, Siga H, Zurek M, Palmér M, Pehrsson S, Albery T, Bomer N, Hoes MF, Boogerd CJ, Frisk M, van Rooij E, Damle S, Louch WE, Wang QD, Fritsche-Danielson R, Chien KR, Hansson KM, Mullick AE, de Boer RA, van der Meer P (2021)
Phospholamban antisense oligonucleotides improve cardiac function in murine cardiomyopathy
Nat Commun, 12 (1), 5180
PubMed 34462437 DOI 10.1038/s41467-021-25439-0
Sadredini M, Haugsten Hansen M, Frisk M, Louch WE, Lehnart SE, Sjaastad I, Stokke MK (2021)
CaMKII inhibition has dual effects on spontaneous Ca2+ release and Ca2+ alternans in ventricular cardiomyocytes from mice with a gain-of-function RyR2 mutation
Am J Physiol Heart Circ Physiol, 321 (2), H446-H460
PubMed 34270372 DOI 10.1152/ajpheart.00011.2021
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