Swiss
Researchers in Zürich are presenting an entirely new view on the mechanisms behind inflammatory heart diseases. The researchers hope to further develop their findings and translate them into clinical setups; Dr. Gabriela Kania and Prof. Urs Eriksson explain more
Unlocking the factors behind inflammatory heart disease
Dr. Gabriela Kania and Prof. Urs Eriksson claim they have significantly contributed to current knowledge about pathophysiological processes occurring in the inflamed heart. Nevertheless, according to Kania,
mechanisms of inflammatory heart disease development, especially in humans, are still poorly understood. Therefore, she says insight from animal models is of upmost importance, particularly with regard to the development of therapeutic strategies against
inflammatory cardiomyopathy (iDCM).
Inflammation studies Inflammation is a fundamental biological process following stress and tissue injuries of any cause, such as viral, autoimmune, ischemic or mechanical stress. The “appropriate response” is expected to
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attenuate injury, enhance survival, accelerate repair and preserve organ function. In contrast, an “inappropriate response” will amplify injury, promote cell death, enhance fibrosis and pathological tissue remodelling accelerating organ failure. Cardiac inflammation – myocarditis – is an important and overall underestimated cause of heart failures, especially in younger patients, Kania explains. For seven and a half years, Kania has been
working on the mouse model of experimental
autoimmune myocarditis
(EAM). Through mice studies, she investigates the mechanistic and physiopathologic aspects of the progression of acute cardiac inflammation into end stage heart failure. She says the end stage heart failure phenotype in mice, following EAM, is morphologically very much similar
to the phenotype observed in humans after infections with cardiotropic viruses. Therefore the EAM model mirrors important pathogenetic aspects of human iDCM. Within the Cardioimmunology group, Dr.
Przemyslaw Blyszczuk leads studies focusing on development and regulation of adaptive immunity in the EAM model. He focuses his projects on cross-talk between antigen presenting cells and autoreactive effector T helper cells, as well as on the molecular mechanisms of heart-specific autoimmunity. He explains, “I plan to elucidate mechanisms of heart-specific autoimmunity in human using “humanised” mouse models. In this context I specifically focus on the regulation of autoreactive T-cell expansion”. Kania summarises “we strongly believe, that several of our recently developed
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