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

Informacje na temat projektu

CureCKDHeart

Identyfikator umowy o grant: 677448

DOI

10.3030/677448

Projekt został zamknięty

Data podpisania przez KE 18 Kwietnia 2016

Data rozpoczęcia 1 Maja 2016

Data zakończenia 30 Kwietnia 2022

Finansowanie w ramach

• EXCELLENT SCIENCE - European Research Council (ERC)

Koszt całkowity

€ 1 497 888,00

Wkład UE

€ 1 497 888,00

Koordynowany przez

UNIVERSITAETSKLINIKUM AACHEN
Germany

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

Okres sprawozdawczy: 2020-11-01 do 2022-04-30

Podsumowanie kontekstu i ogólnych celów projektu

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.

Prace wykonane od początku projektu do końca okresu sprawozdawczego oraz najważniejsze dotychczasowe rezultaty

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.

Innowacyjność oraz oczekiwany potencjalny wpływ (w tym dotychczasowe znaczenie społeczno-gospodarcze i szersze implikacje społeczne projektu)

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