Norbert Frey

This study shows that HDAC inhibition with SAHA reduces doxorubicin-induced cardiotoxicity by modulating Topo IIb and MEF2-dependent transcription.

The paper describes an ex vivo study using normothermic machine-perfused human hearts to evaluate AAV-mediated gene delivery for cardiac gene therapy.

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 identifies FYCO1 as a regulator of autophagy that improves cardiac remodeling after myocardial infarction by enhancing autophagic flux and reducing inflammation.

This study shows CD47 blockade reprograms the monocyte-macrophage axis in atherosclerosis, reducing inflammation and enhancing apoptotic cell clearance.

This study shows that cardiomyocyte autophagy promotes a pro-regenerative immune response by modulating macrophage gene expression during zebrafish cardiac regeneration.

This study shows cardiomyocytes use GBP5 to regulate both pro- and anti-inflammatory responses to IFNγ through the AIM2/CASP1 pathway and GBP5/TGFβ axis.

This study identifies MLP as a non-canonical RNA-binding protein in cardiomyocytes and shows its RNA-dependent interaction with cytoskeletal complexes.

This study shows that loss of eEF1A2 in cardiomyocytes causes cardiomyopathy through proteostasis defects, and mTORC1 inhibition can reverse the condition.

The paper uses single molecule long-read sequencing to analyze transcriptomes in heart failure patients and controls, identifying novel isoforms and convergent isoform changes across different cardiomyopathy types.

This study shows that reverse cardiac remodeling is a constrained multicellular state with partial recovery of metabolic programs but persistent inflammatory-mitochondrial dysfunction, mediated by lymphatic-derived Reelin.

This study identifies TRIM24 as a chromatin regulator that suppresses inflammatory signaling in cardiomyocytes, preventing cardiac inflammation and heart failure progression.

This paper integrates bulk and single-cell transcriptomic data from 25 heart failure studies to identify conserved multicellular coordination patterns in cardiac remodeling.

This study investigates ZEB1's role in cardiomyocyte structure and function, finding that its deletion causes sarcomere damage, mitochondrial dysfunction, and dedifferentiation, particularly in females.

The paper curates a cross-species multimodal database of gene expression in cardiac hypertrophy and introduces an interactive web tool for exploring gene expression across multiple omics layers.

This study introduces AB2, a photochromic ligand that modulates cardiac electrophysiology via light, converting ventricular arrhythmias into sinus rhythm in an ex-vivo heart model.

This study identifies Gadlor1 and Gadlor2 as endothelial cell-derived lncRNAs that worsen cardiac remodeling through EV-mediated crosstalk with cardiomyocytes.

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.

This study shows that Ythdf2, an m6A reader protein, regulates cardiac function by controlling gene expression through its target transcripts, leading to cardiac remodeling in heart failure models.

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.

This study performs a genome-wide association analysis of hemorrhoidal disease in 944,133 individuals, identifying 102 risk loci and linking them to vascular and tissue development pathways.