InRegen · Fine-tuning the inflammatory response following cardiac injury to promote cardiac regeneration
Horizon 2020 — Marie Skłodowska-Curie Actions
- Duration
- 2021-03-15 → 2023-03-14
- EU contribution
- €153,085
- Participants
- 1
- Scheme
- MSCA-IF
Lines connect the coordinator with its partners.
Results in brief
Fine-tuning the inflammatory response following cardiac injury to promote cardiac regeneration
Myocardial infarction-related heart failure is a major cause of high mortality. Innate immunity, specifically macrophages and neutrophils, plays a crucial role in heart injury, scar regression, and regeneration. Neutrophils are among the first immune cells recruited to the site of injury, where they clear debris and release molecules that attract macrophages. Macrophages are also involved clearing dead cells, promoting angiogenesis and tissue repair, and contributing to fibrotic tissue formation. Macrophages communicate with other cells through various secreted molecules, including cytokines, chemokines, and extracellular vesicles, which influence recipient cell behaviour. Achieving a balance between innate immunity activation and resolution is crucial for cardiac tissue repair and preventing excessive inflammation and tissue damage. Zebrafish, known for its regenerative abilities, provides a model for studying heart regeneration. Upon heart injury, zebrafish exhibit a controlled inflammatory response involving macrophages and neutrophils, which clear damaged tissue and promote regeneration. Understanding the mechanisms underlying heart regeneration in zebrafish may provide insights for potential therapeutic strategies heart failure.
Data: CORDIS, © European Union
Project objective
The pronounced inability of adult human/mammalian heart to regenerate causes millions of deaths following cardiac insult, particularly in the longer term. The extent and persistence of associated inflammation has been generally linked with adverse cardiac outcomes, including fibrosis, hypertrophy, and dysfunction. However, characteristics of the inflammatory response e.g. the maturity of resident macrophages and/or the activation status of infiltrating cells may differentially influence cardiac fibroblasts and, most importantly, cardiomyocytes, thus affecting cardiac regeneration, hypertrophy, fibrosis and dysfunction. Unraveling crucial parameters of such interactions in appropriate biological systems should confer decisive intervention potential in a serious health problem. In the past years we have studied in detail cellular and molecular players regulating pivotal events initiating or sustaining the progress to heart failure (HF) in mice and zebrafish and we propose here to combine the systems to globally study these interactions.
Original text from CORDIS.
Participants
- IDRYMA IATROVIOLOGIKON EREUNON AKADEMIAS ATHINON · AthinaCoordinatorGreece
Links
Data: CORDIS, © European Union