Redox and nitrosative regulation of cardiac remodeling: novel therapeutic approaches for heart failure
- Ajay M. SHAH, King's College, London (UK)
- David A. KASS, Johns Hopkins University, Baltimore (USA)
- Ivor BENJAMIN, Medical College of Wisconsin, Milwaukee (USA)
- Barbara CASADEI, University of Oxford (UK)
- Philip EATON, King’s College, London (UK)
- Junichi SADOSHIMA, Rutgers University, Newark (USA)
- Lothar BLATTER, Rush University Medical Center, Chicago (USA)
- Keith CHANNON, University of Oxford (UK)
- Judith HAENDELER, University of Düsseldorf (Germany)
- Emilio HIRSCH, University of Torino (Italy)
- Lars MAIER, University Hospital Regensburg (Germany)
- Brian O’ROURKE, Johns Hopkins University, Baltimore (USA)
- Jean-Sebastien SILVESTRE, Paris Center for Cardiovascular Research INSERM U970 (France)
Reactive oxygen and nitrogen species are natural byproducts of normal cellular metabolism. Having unpaired electrons, these molecules tend to capture electrons from proteins, lipids, sugars and DNA to form a more stable electron pair, thus damaging the cell. Normally, reactive oxygen and nitrogen species are neutralized by antioxidant enzymes in a reaction called reduction. However, if the reactive species are present in excessive amounts, they become toxic to the cell, causing oxidative/nitrosative stress.
This network will investigate oxidative/nitrosative stress in patients with heart failure. The network will identify the sources and regulators of reactive oxygen and nitrogen species, elucidate how they cause cardiac dysfunction, and apply the discoveries to design new heart failure treatments. The network members will collaborate using various assays of oxidative/nitrosative stress, small and large animal models of heart failure, and human cardiac tissue samples.