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TP 8 Molecular Mechanism of Heart Failure

Background

We are far from being able to treat the causes of heart failure in patients, let alone heal them. This is primarily because the significance of molecular, pathophysiologically relevant processes has been only inadequately reviewed in experimental models up to now. Our subproject is intended to change this and is working on selected signal cascades and key molecules and their pathophysiological significance in the regulation of hypertrophy, cell division, survival and function of cardiac muscle cells as the basis for the development of heart failure. In addition, we are working on a series of known and newly-identified secretory factors that are responsible for the communication between the different types of cells in the failing heart.

Objective

The purpose of this subproject is to utilize molecular biological research to develop prerequisites for innovative intervention strategies which can be used as the foundation for innovative treatment approaches for patients with heart failure.

Main result

Several important protein molecules (e.g. MLP, ARC, GDF-15) were characterized with regard to their importance for disease initiation, progression and modification in heart failure.

Publications

  • Heineke J et al. Attenuation of cardiac remodeling after myocardial infarction by muscle LIM protein-calcineurin signaling at the sarcomeric Z-disc. Proc Natl Acad Sci USA. 2005;102:1655-60.
  • Donath S et al. Apoptosis repressor with caspase recruitment domain is required for cardioprotection in response to biomechanical and ischemic stress. Circulation. 2006;113:1203-12.
  • Kempf T et al. Prognostic utility of growth-differentiation factor-15 in patients with chronic heart failure. J Am Coll Cardiol. 2008;50:1054-60.

Perspective

Several spin-off research projects were initiated based on the subproject 8. Currently, in a cooperation with Roche Diagnostics, a test system for GDF-15 is developed in order to better predict the course of disease and prognosis in heart failure. Further, the identified molecules and signalling pathways are expected to yield innovative diagnostic and therapeutic options in the near future.

Contact

Prof. Dr. Kai Wollert
Medizinische Hochschule Hannover
Klinik für Kardiologie und Angiologie
Phone: +49 (0)511 5324055
E-Mail: ed.revonnah-hmnull@iak.trellow