pathogenic principles could be generalized to other heart diseases as well, including ischemic heart disease”.
New view The group’s findings offer an entirely new view to the mechanisms behind heart disease course. “The group realised pretty quickly that stem cell based therapies had no future in heart inflammatory disease ,as the inflammatory environment always dictates the fate of the precursor cells,” Eriksson says. “In the past, researchers have not made
a connection between inflammation and fibrosis. But we’ve found that inflammatory cells basically contain
infiltrating inflammatory cells,” he says. “We then have to work out how to target
the heart and which drugs will influence this remodelling process.”
Group Eriksson set up the Cardioimmunology research group after receiving a Swiss National Foundation professorship first in Basel (University Hospital) in 2004, and later, in 2008 moved it into Zurich University, joining as the research group leader and heart failure consultant for the Department of Cardiovascular Research headed by Prof. Thomas F. Lüscher. Although today the professor has taken a step back to focus on his role as head of
Project Information AT A GLANCE
Project Title: Myocardial inflammation: Unlocking the factors behind inflammatory heart disease
Project Objective: Successful completion of our projects will advance our understanding of myocardial inflammation and its progression into inflammatory cardiomyopathy, and contribute to the development of novel therapeutic strategies. Moreover, we expect to reveal general mechanistic principles, which can apply to other heart diseases associated with strong inflammatory responses.
“We strongly believe, that several of our recently developed pathogenic principles could be generalized to other heart diseases as well, including ischemic heart disease”
large amounts of non-committed precursors which have the capacity to differentiate into myofibroblasts and therefore represent the cellular substrate of fibrotic tissue remodeling in iDCM.” The group’s previous studies have identified inflammatory
CD133+
progenitor cells as the key compartment of
pathological remodelling in
inflammatory heart disease and point to the critical role of epigenetic factors in this process. Kania says that the most recent research has been fairly ground breaking, showing that a single hematopoietic cytokine modulates post- inflammatory fibrogenesis and heart failure progression by affecting progenitor cell fate and function. Eriksson expects that if the team can
specifically target these inflammatory cells to prevent their transition into pathological myofibroblasts, they could then block the development of a phenotype of end stage heart failure. “This is really a big step forward because
all these fancy treatments, like stem cell treatment and so on, do not convincingly work in practice yet. Of course it’s tempting to design such strategies, but I believe the smartest, certainly the fastest approach is
to look at what we have
available as active compounds and then check how those drugs may influence the phenotype
and 34 fate of early heart-
Department of Medicine at the GZO -Zurich Regional Health Centre, he continues to push and expand his research and
participates in the educational
activities of the Zurich University. Eriksson, Drs. Kania and Blyszczuk
design, supervise and perform all cardioimmunology research projects and organize all the funding for the group, 30 per cent of which comes from the Swiss National Foundation, while another 30 per cent from other foundations, such as the Swiss Heart Foundation, Holcim, Olga Mayenfich or Hartmann Müller Foundations. A large chunk of funding, however, also comes from the GZO - Zurich Regional Health Center, in a bid to keep strong links between the University and one of the most important and rapidly growing hospitals in the greater Zurich area, he explains.
Future goals Kania says “until
recently we focused
mostly on the role of epigenetic factors influencing the inflammatory progenitors and the transition from the acute to the chronic pathological phase in iDCM. In the near future we aim to address the role of genetic factors in EAM development and the progression of post-inflammatory iDCM as well.” The group’s main focus of the ongoing research is to “move from basic science
Contact: Tel: +41 44 635 49 95 Email:
gabriela.kania@uzh.ch urs.eriksson@
gzo.ch
Web:
www.zihp.uzh.ch/aboutus/members.html www.physiol.uzh.ch/research/ CardiovascularResearch.html
www.gzo.ch
Insight Publishers | Projects
Dr. Gabriela Kania Head, Division of Cardioimmunology, Cardiovascular Research, Institute of Physiology, University of Zürich
Project Duration and Timing: Our research contains several projects that have been studying since 2006 till today.
Project Partners: Dr. Przemyslaw Blyszczuk
Main Contact:
Contact
Prof. Dr. med. Urs Eriksson Chairman, Department of Medicine, Zurich Regional Health Center - GZO AG, Spitalstrasse 66, 8620 Wetzikon & Division of Cardioimmunology, Cardiovascular Research, Institute of Physiology, University of Zürich
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