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Clonal hematopoiesis (CH) is a common age-related condition characterized by the outgrowth of mutated hematopoietic clones which can lead to life-threatening malignancies. CH is caused by mutations in hematopoietic stem cells (HSCs) and is accelerated in individuals with ischemic hearth failure. This DFG funded project aims to define the key bone marrow components and cell-extrinsic signais involved in promoting CH following hearth failure. Using established animals models, patient cohorts and cutting-edge single-cell quantitative biology, we will uncover the underlying mechanism of targeted candidate signals from bonw marrow niches. Our goal is to leverage those findings towarsds the design of novel therapeutic strategies to decelerate outgrowth of mutated hematopoietic clones.