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Funder/CentreGerman Research Foundation (Deutsche Forschungsgesel...
Programme:Cardiac Failure in the Elderely: cellular mechanisms...
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Cardiac Failure in the Elderely: cellular mechanisms and therapeutical targets (SFB 598)Research Programme


Programme type

Research programme

Programme status


Total number of funded projects


Summary of key aims

Cardiac failure is not a monocausal disease but a syndrom starting from different etiologies. Complex cellular, neurohumoral and hemodynamic interactions of the cardiomyocytes with the whole organism result in a progression of the syndrom. Finally, cardiac failure can lead to death due to progressive pump failure or due to fatal ventricular arrhythmias. The current therapies availabe can slow down this development but they do not prevent it. As a result, more than 30% of the population above 65 years is living with cardiac failure of variable severity. This number and its fiscal burden will increase with the increasing age of society. The mechanisms that drive the aged heart into failure, not clear at present, shall be analysed in our project grant. We hypothesise that cardiac ageing starts with the death of indiviual myocytes, caused by mutations of mitochondrial genes and by the effect of reactive oxygen species that damage DNA in mitochondria and nucleus as well as proteins in the cell and the extracellular matrix. We will study how the reduced population of cardiomyocytes can adapt to this situation by expressing hypertrophy-associated genes, on expense of their phenotype plasticity. We will study how sustained mechanical or metabolic stress, exceeding the limits of the reduced adaptability, induces indiviual myocytes to fail and to die. The myocyte population is further reduced, the ventricular wall thins, dilates and secrets neurohormones into the blood that modulate heart and body similarly to an inflammatory syndrom. We shall analyse these signals. If the cardiac function cannon adequately be mainitained in spite of these reactions, the heart will fail, either during exertion or even at rest. We try to interfere with the development of failure of reactivating mitotic signals in the non-dividing adult cardiomycytes, recovering the number of regenerating destroyed ventricular tissue. The results of our basic research shall be transferred into relevance for the aged population. To this end, caridac phenotype and function of a representative sample of 1750 male and femal volunteers (age between 45 and 80 years) will be characterised with focus on the heart rate variability. This parameter, easily measurable from ECG, shall be established as a marker for early diagnosis of the developing cardiac failure, useful for the management of the elderly with regard to prevention and therapy of heart failure.

Management contact

Stefan Lohwasser
Kennedyalle 40
53175 Bonn

Scientific contact

Gerrit Isenberg
+49 345 55 20
Martin-Luther-Universitat Halle-Wittenberg
Magdeburger Strasse 6
06112 Halle

Funding contact

Deutsche Forschungsgemeinshcaft
Kennedyallee 40
53175 Bonn

Is the project externally evaluated?


Who has evaluated, or will evaluate, the programme?


What forms of international collaboration does the programme support?

  • ▪ Foreign collaborators working in their own countries
  • ▪ Travel for foreign collaborators
  • ▪ National researchers abroad
  • ▪ Travel for national researchers

Interdisciplinary research is a strategic priority...

  • For the programme ✔
  • For the funding agency ✔
  • Nationally ✔