Public Defence: Kine Andenæs

MSc Kine Andenæs at Institute of Clinical Medicine will be defending the thesis “Translational cardiac research: Importance of the matrix molecules fibromodulin and lumican in left ventricular pressure overload” for the degree of PhD (Philosophiae Doctor).

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Photo: Roy Trondsen

Due to copyright reasons, an electronic copy of the thesis must be ordered from the faculty. In order for the faculty to have time to process the order, it must be received by the faculty no later than 2 days prior to the public defence. Orders received later than 2 days before the defence will not be processed. Inquiries regarding the thesis after the public defence must be addressed to the candidate.

Trial Lecture – time and place

See Trial Lecture.

Adjudication committee

  • First opponent: Professor Marion Kusche-Gullberg, University of Bergen
  • Second opponent: Senior Researcher Mona Elisabeth Pedersen, Nofima
  • Third member and chair of the evaluation committee: Associate Professor Jørgen Gravning, University of Oslo

Chair of the Defence

Professor Thor Edvardsen, University of Oslo

Principal Supervisor

Professor II Theis Tønnessen, University of Oslo


Heart failure is a common, deadly and highly morbid syndrome. When the heart is exposed to stimuli such as pressure overload, it remodels. The aim of this thesis was to examine the role of the extracellular matrix proteoglycans fibromodulin and lumican in cardiac remodeling in response to cardiac pressure overload. These molecules bind to fibrillar collagens in the matrix surrounding the cardiomyocytes in the heart, and are thought to be involved in wound healing and scarring. Cardiac fibrosis is a central remodeling process of the heart, impairing cardiac function. Thus, a better understanding of proteoglycans such as lumican and fibromodulin is of importance, to be able to develop improved treatment for heart failure patients in the future.

We used gene-modified mice to examine how lack of lumican or fibromodulin affected cardiac remodeling when mice were subjected to experimental cardiac pressure overload. We also performed in vitro overexpression experiments in cardiac cells.

Cardiac levels of fibromodulin and lumican were increased in failing hearts. Our results show that even though fibromodulin and lumican are part of the same family of proteoglycans, they have contrasting effects in the failing heart. Mice lacking fibromodulin developed a mildly exacerbated hypertrophy during pressure overload, with no difference in mortality or fibrosis. Meanwhile, mice lacking lumican had high mortality and developed severe dilated heart failure with thin walls, impaired contraction and reduced fibrosis. In cultured cardiac fibroblasts, including human cells, fibromodulin reduced fibroblast migration and the expression of fibrosis-related proteins, suggesting an anti-fibrotic role. In cultured cardiac fibroblasts, lumican increased expression of fibrosis-related molecules including miR-21, suggesting a pro-fibrotic role. Our research contributes with insight into the molecular mechanisms underlying cardiac remodeling and failure.

Additional information

Contact the research support staff.

Published Apr. 19, 2022 12:32 PM - Last modified May 2, 2022 4:03 PM