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Hypertonie und kardiovaskuläre Endorganschäden


Prof. Dr. Reinhold Kreutz

Leiter des Schwerpunktbereichs


Prof. Dr. Reinhold Kreutz


Charite; Universitätsmedizin Berlin / Campus Benjamin Franklin

Institut für Klinische Pharmakologie und Toxikologie

Abteilung Klinische Pharmakologie

Hindenburgdamm 30

12200 Berlin

email:  reinhold.kreutz@charite.de

Tel:     030-8445 2279




Arterial hypertension is one of the most important risk factors for cardiovascular morbidity and mortality. Recent epidemiological analyses show that the prevalence of arterial hypertension increases dramatically in Germany and also world wide. The clinical importance of arterial hypertension is associated with the resulting cardiovascular damages. Experimental and clinical data reveal the genetic role in the manifestation and progression of cardiovascular damages following arterial hypertension. The main goal of the research project is the characterization of the genetic and molecular background of hypertensive end organ damage in the heart and  arterial vessels.


By means of an integrated analytical approach the pathomechanisms of functional and structural organ damages are analyzed on the molecular level. Our analyses encompass experimental approaches in genetic modified models of mouse and rat. One main research topic is the genome wide association study in polygenetic animal models with left ventricular hypertrophy and dysfunction in the rat. New candidate genes for left ventricular damage in humans shall be identified by comparative genome analyses. These analyses where made possible by established network structures within topic CV1.3 which allow a wide spectrum of functional analyses of identified candidate genes. We carry out experimental analyses in cell culture and isolated organs as well as by in vivo studies involving Zebra fish, mouse and rat models.  Additional clinical and functional analyses areperformed in selected patients with hypertension and end organ damage. The data are confirmed by genetic analyses in larger population. Our research program shall contribute to the characterization of new target genes for diagnostics and therapy of hypertensive end organ damage.



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