Karl Swärd


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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.


Expertise related to UN Sustainable Development Goals

In 2015, UN member states agreed to 17 global Sustainable Development Goals (SDGs) to end poverty, protect the planet and ensure prosperity for all. This person’s work contributes towards the following SDG(s):

  • SDG 3 - Good Health and Well-being

UKÄ subject classification

  • Physiology


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