Florian Leuschner

This study shows that FAP-targeted BiTE(R) molecules, intended to reduce cardiac fibrosis, instead worsen heart function by triggering harmful immune responses.

This study identifies mitochondrial metabolic inflexibility and S-nitrosylation remodeling in a murine HFpEF model and shows ketone supplementation partially rescues metabolic and functional defects.

This study identifies a cardio-intestinal innate immune circuit driven by tricuspid valve regurgitation that promotes heart failure through IL-6-mediated myocardial fibrosis and dysfunction.

This study compares two myocardial infarction models, showing the intact-chest model better reflects human immune responses and identifies immature neutrophils as contributors to cardiac dysfunction.

The paper develops a method to isolate intact engineered extracellular vesicles with high purity using twin-Strep tagging and Strep technology, enabling efficient and selective capture and functional delivery of proteins.

This study identifies RUNX1 as a key regulator of cardiac recovery by reprogramming macrophages, showing that its inhibition promotes heart function recovery in a chronic heart failure model.

This study shows that DNMT3A mutations in CHIP lead to metabolic changes in macrophages that drive inflammation, and targeting these changes can improve heart failure outcomes.

This study maps acute murine myocardial infarction with subcellular resolution, identifying a novel endocardial route of immune cell infiltration and vWF as a key mediator.

The paper defines the cellular and transcriptional features of cardiac recovery using snRNA-seq, identifying RUNX1 downregulation as a key predictor and potential therapeutic target.

This study shows that temporarily inhibiting protein translation after heart attack reduces inflammation and improves long-term heart function by targeting the mTORC1-4EBP1-eIF4F pathway.