Karl Swärd

Professor

Research areas and keywords

UKÄ subject classification

  • Physiology

Research

By unraveling mechanisms by which hypertension translates into cardiovascular disease we hope to identify novel targets for therapy. Mechanical forces exerted by an elevated blood pressure are sensed and translated into biochemical signals by multiple mechanisms. In one project we have discovered that hypertension feeds into the NOTCH signaling pathway, heavily burdened by mutations in human stroke syndromes. This establishes a hitherto unknown mechanistic link between hypertension-driven stroke and syndromic stroke.

Caveolae are membrane organelles considered to play a mechanoprotective role. In another project we characterize mice that lack critical building blocks for caveolae with a view to understand a group of diseases referred to as caveolinopathies. In recent work, we identified what appears to be a critical genetic on-off switch for formation of caveolae: myocardin family coactivators. Current efforts focus on the details of this genetic control mechanism.

One of the most mechanoresponsive genes in the genome is thrombospondin-4 (Thbs4). Thbs4 encodes a matrix protein that also functions as an upstream activator of one arm of the unfolded protein response. We have discovered that mutant mice lacking Thbs4 develop maladaptive remodeling of the heart in Angiotensin II-driven hypertension. They are also strikingly susceptible to aneurysm development. We now try to understand the mechanistic basis of these phenotypes.

Research

Recent research outputs

Dahan, D., Thi Hien Tran, Tannenberg, P., Ekman, M., Catarina Rippe, Boettger, T., Braun, T., Karin Tran-Lundmark, Tran, P., Karl Swärd & Sebastian Albinsson 2017 Aug 11 In : Journal of Vascular Research. p. 246-256 11 p.

Research output: Contribution to journalArticle

View All (88)