Nadja Sachs

This study uses Deep Visual Proteomics to analyze VSMC phenotypes in atherosclerotic plaques, finding spatially distinct phenotype distributions and a shift toward dedifferentiated states in unstable plaques.

This paper shows that blocking endothelial CB1 receptors reduces arterial inflammation and lipid uptake under atheroprone shear stress, suggesting potential therapeutic benefits for atherosclerosis.

COSIE is a computational framework that integrates multiple spatial omics modalities to generate high-resolution molecular landscapes, outperforming existing methods across diverse datasets.

HistoSweep improves tissue quality control in gigapixel images by removing artifacts and preserving biologically relevant structures, enhancing analysis accuracy in digital pathology and spatial omics.

This study shows cancer increases atherosclerotic plaque vulnerability through pathological angiogenesis, and targets this pathway to prevent plaque destabilization.

This study integrates single-cell spatial transcriptomics with bulk and single-cell RNA sequencing to reveal the molecular heterogeneity and mechanisms of atherosclerotic carotid artery plaques.

This study identifies nuclear eNOS's role in modulating ADAR1 activity and type I interferon signaling, linking NO bioavailability to endothelial function and atherogenesis.

This study creates an integrated single-cell atlas of human atherosclerotic plaques using scRNA-seq data, enabling accurate cell type annotation and downstream analyses.

This study identifies CCR2+ neutrophils in atherosclerotic plaques that promote instability through ROS production and NET release, and shows that targeting CCR2 reduces plaque destabilization.

The paper identifies self-reactive B cells in atherosclerosis-associated tertiary lymphoid organs that produce high-affinity autoantibodies contributing to disease progression.

The paper identifies cATM as a circRNA upregulated in AAA tissue and patient-derived SMCs, showing its role in oxidative stress adaptation and potential as a biomarker for AAA.

This study identifies NUDT6 as an antisense transcript of FGF2, showing that its silencing enhances smooth muscle cell survival and limits vascular disease progression.

This study identifies ADAMTS-7 as a risk factor for atherosclerosis by degrading TIMP-1, reducing its inhibition of MMP-9 and promoting collagen degradation.