Research Unit 5953 Intervening in the Innate Immune Response early after Myocardial Infarction
A myocardial infarction immediately triggers a strong inflammatory response that critically influences tissue healing and the extent of scar formation. The ETNA consortium is developing targeted immunomodulatory strategies to modulate the functions of neutrophils and macrophages early after myocardial infarction, with the aim of limiting harmful inflammatory responses while supporting mechanisms that promote healing.
Intervening in the Innate Immune Response early after Myocardial Infarction
Following myocardial infarction, the innate immune system plays a central role in the repair of damaged cardiac tissue. In particular, neutrophils and macrophages can either exacerbate tissue damage or promote healing, depending on their activation state. Previous therapeutic approaches aimed at broadly suppressing inflammation have shown only limited success.
ETNA therefore pursues a new, targeted approach: rather than blocking inflammation as a whole, specific populations of the innate immune system will be precisely modulated at the appropriate time during the healing process. To this end, the functions, dynamics, and phenotypic changes of neutrophils and macrophages will be investigated and suitable pharmacological strategies developed. Particular emphasis will also be placed on sex-specific differences in the immune response and clinical course following myocardial infarction.
The long-term goal is to improve healing after myocardial infarction, prevent the development of heart failure, and establish new precise therapeutic approaches for patients.
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