SMART

Systems Medicine of Heart Failure

The onset and course of heart failure (HF) is triggered by a complex regulatory network that includes stressors (pressure overload by individual anatomic hemodynamic settings), intrin-sic (genes), environmental (regulating epigenetics), and modifying factors (such as hor-mones and the immune system). SMART aims to establish individualized strategies for the prevention and management of HF by early detection of the physiological, genomic, proteo-mic and hemodynamic mechanisms that lead from onecommon cause of ventricular dys-function (pressure overload) to maladaptive remodelling and irreversible HF. To cope with the complexity of HF, SMART will interrelate models describing the interplay between ge-nome, proteome and cell function, regulating hormones, tissue composition and hemody-namic whole organ function up to a whole body description of a patient and patient cohorts. The ultimate goal is to demonstrate proof-of-concept tools for predicting disease evolution and efficacy of treatment in a given patient. To achieve this task SMART will apply
- A modelling framework that couples multi-scale mechanistic models with in-depth genome/proteome, cell physiology and whole organ (biomechanical and fluid dynamic) models
- Subsequently, investigate methods validity and relevance for “quantitative prediction” of treatment outcome in a clinical proof-of-concept trial (demonstrator) of patients with aortic valve desieases.
 

The consortium joins some of Germany’s most prestigious institutes and companies

• Multilevel Modelling: Max-Delbrück Center, Bayer Technology Services GmbH, Deutsches Herzzentrum Berlin
• Omics: Max-Delbrück Center
• Genetic: Charité-University Medicine Berlin
• ICT and Bioinformatik: Hasso-Plattner-Institut
• Clinical science: Deutsches Herzzentrum Berlin and Charité-Universitätsmedizin Berlin

 

Subprojects in SMART: 

SP 1   Systems Medicine of Heart Failure

SP 2   Real-Time Analysis of Genome Data using In-Memory Database Technology

SP 3   Transcriptome and miRNAome analysis in native and Ang II treated human myocardium

SP 4   Cell physiology modelling and proteomics

SP 5   Image based modelling (DHZB/Charite)

SP 6   Mechanistic multiscale models

Keywords: cardiovascular diseases