Stefanie Dimmeler

The paper examines age-related clonal hematopoiesis and mosaic sex chromosome loss in UK Biobank participants, finding distinct proteomic programs and disease associations for each.

This study identifies SNHG29 and IGF2BP1 as a lineage-specific oncogenic circuit in AMKL, showing their dependency and therapeutic vulnerability.

The paper introduces a temporal AI model, MaxToki, trained on extensive gene data to predict cell state changes across human aging and identifies age-modulating targets.

This study identifies polyploid cardiomyocytes as disease-specific transcriptional states in the mammalian heart and suggests targeting them for heart failure treatment.

This paper identifies immunomodulatory endothelial cells (IMEC) that present antigens on MHC class II and activate T cells in atherosclerosis.

The paper uses human heart organoids to model mitochondrial disease and identifies a drug that improves mitochondrial function and tissue contractility.

The paper identifies the transaminase-omega-amidase pathway as a redox-sensitive metabolic switch in endothelial glutamine metabolism, showing that NIT2 oxidation inhibits its activity and affects angiogenesis.

This study shows that loss of KDM6A in hematopoietic cells impairs cardiac recovery after heart failure by causing epigenetic changes in myeloid cells that increase inflammation and worsen cardiac outcomes.

This paper uses single-nucleus RNA sequencing to analyze HFpEF myocardium, identifying transcriptional changes in cardiomyocytes, endothelial cells, fibroblasts, and macrophages that suggest metabolic, inflammatory, and fibrotic mechanisms.

This study identifies differentially explained genes in heart failure subtypes using neural networks and XAI tools to improve understanding of molecular mechanisms.

This study identifies vascular niches as key hotspots for age-related inflammation and fibrosis in cardiac tissue using single-nucleus RNA sequencing and spatial transcriptomics.

This study identifies adventitial leptin receptor-expressing fibroblasts as key contributors to cardiac fibrosis after myocardial infarction in mice and humans.

This study identifies ZBTB16 as a critical regulator of endothelial function in aging, showing its protective role against cardiac dysfunction through suppression of pro-fibrotic signaling.

The paper identifies reduced STAT3 expression in cardiac pericytes in HFpEF and shows its loss leads to senescence and impaired adhesion.

This study identifies decorin as a factor induced by aging that contributes to cardiac inflammation and diastolic dysfunction through pro-inflammatory effects in the myocardium.

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 paper identifies MIRIAL as an aging-induced lncRNA that regulates endothelial quiescence and mitochondrial function through a novel triplex mechanism.

This study identifies the lncRNA Sweetheart as essential for compensatory cardiac hypertrophy after myocardial injury, working synergistically with NKX2-5.

The paper identifies regulatory SNPs linked to CVDs and shows their impact on non-coding RNA expression and cardiac function in disease models.

This study identifies circPLOD2 as a hypoxia-regulated circRNA that modulates pericyte function by regulating KLF4, affecting proliferation and vascular interactions.

The paper introduces a cross-species integration pipeline for scRNA-seq data, validated on heart failure datasets from mice and humans, improving ortholog assignment and enabling pathway comparison.

This study shows that DOT1L regulates specific gene networks in cardiac development and cell cycle withdrawal through H3K79me2 modifications.

This study compares common scRNA-seq alignment tools, finding differences in runtime, cell and gene detection, and potential artifacts, highlighting the impact of mapping strategies on analysis outcomes.

This study identifies the PNUTS-PP1 axis as critical for endothelial aging and barrier function, showing that SEMA3B suppression mediates these effects.