Molecular and cellular changes during development of cardiac fibrosis in cardiomyopathy

• Applicant: Dr. Daniel Reichart
• Subject Area: Cardiology, Angiology
• Term: from 2018 to 2020
• Project identifier: Deutsche Forschungsgemeinschaft (DFG) - Project number 413001050

Cardiomyopathies are a heterogeneous group of diseases, characterised by pump failure and malignant arrhythmias; they are frequently associated with genetic abnormalities. Mortality is high and up to 45-60% within the first 5 years after diagnosis. Therapeutic options include multimodal medical treatments, biventricular pacemakers, mechanical assist devices and heart transplantations. Abundant pathologic development of fibrosis is a crucial histologic (and pathophysiological) feature of all cardiomyopathies. Fibrosis is caused by an increased production and decreased degradation of the extracellular matrix (mostly collagen), which finally causes cardiac adverse remodeling. These myocardial structural changes are associated with systolic and/or diastolic dysfunctions and arrhythmias. Recent investigations proved that fibroblasts and cardiac macrophages are the major pathologic drivers due to their common transcriptional changes; these changes, however, differ in between different types of cardiomyopathies. The research work in Boston will therefore focus on the origins/migrations of fibroblasts and cardiac macrophages, their molecular activation/suppression pathways and last but not least on possible therapeutic targets.

• DFG Programme: Research Fellowships
• International Connection: USA
• Hosts: Professorin Christine E. Seidman; Professor Jonathan G. Seidman, Ph.D.