Targeting perivascular myofibroblast progenitors to treat cardiac fibrosis and heart failure in chronic kidney disease

Información del proyecto

CureCKDHeart

Identificador del acuerdo de subvención: 677448

DOI

10.3030/677448

Proyecto cerrado

Fecha de la firma de la CE 18 Abril 2016

Fecha de inicio 1 Mayo 2016

Fecha de finalización 30 Abril 2022

Financiado con arreglo a

• EXCELLENT SCIENCE - European Research Council (ERC)

Coste total

€ 1 497 888,00

Aportación de la UE

€ 1 497 888,00

Coordinado por

UNIVERSITAETSKLINIKUM AACHEN
Germany

Periodic Reporting for period 4 - CureCKDHeart (Targeting perivascular myofibroblast progenitors to treat cardiac fibrosis and heart failure in chronic kidney disease)

Período documentado: 2020-11-01 hasta 2022-04-30

Resumen del contexto y de los objetivos generales del proyecto

Chronic kidney disease (CKD) is a growing public health problem and affects more than 10% of the population in Europe. CKD patients suffer from massively increased cardiovascular morbidity and mortality. This is due to vascular calcification and atherosclerosis as well as cardiac remodeling with fibrosis, hypertrophy and capillary loss. The cellular and molecular mechanisms of vascular and cardiac remodeling in CKD are incompletely understood. The major goal of the project are to dissect cellular and molecular mechanisms of kidney and cardiac remodeling and fibrosis and to develop novel interventional strategies to treat patients.

Trabajo realizado desde el comienzo del proyecto hasta el final del período abarcado por el informe y los principales resultados hasta la fecha

We have established several novel high-throughput single cell genomic and spatial transcriptomic technologies to dissect cellular and molecular mechanisms of cardiac remodeling in CKD and aging. Furthermore, we have performed genetic fate tracing experiments in cardiac remodeling in CKD and non-CKD to understand the cell-populations that contribute to cardiac remodeling. We have started to combine genetic fate tracing with single cell genomics to understand cell-heterogeneity and cross-talk in homeostasis and disease. We have generated several large datasets of human and mouse heart and kidney single cell genomic and spatial transcriptomic data and discovered novel mechanisms and identified therapeutic targets.

Avances que van más allá del estado de la técnica e impacto potencial esperado (incluida la repercusión socioeconómica y las implicaciones sociales más amplias del proyecto hasta la fecha)

We have identified and validated several therapeutic targets and are currently developing novel drugs against these targets. In screening experiments we already identified very promising drug candidates.

CureCKDHeart Figure