Lars Mäegdefessel

This study identifies IKKβ activation as a transient upstream signal triggered by efferocytosis that promotes tissue resolution through multiple downstream pathways.

This paper identifies PACERR as a lncRNA that regulates COX-2 and cholesterol transport genes, linking inflammation and cholesterol homeostasis through distinct mechanisms in response to HDL and LPS.

The paper shows that cytokinesis arrest in macrophages leads to binucleation, which enhances efferocytic function and reduces autoimmune responses.

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.

This study identifies desert hedgehog (DHH) as a resilience factor that prevents atherosclerosis by inhibiting PAI-1 signaling and endothelial mesenchymal transition.

The paper identifies 1,580 cell type-specific genes and non-coding RNAs associated with coronary artery disease by integrating genetic and epigenetic data from multiple cell types.

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 shows cigarette smoke increases vascular ADAMTS7 expression through CCL17-CCR4 signaling, linking smoking to atherosclerosis via a novel gene-environment interaction.

This study shows PRDM16 maintains SMC identity and regulates atherosclerotic plaque composition by inhibiting synthetic gene programs during SMC fate switching.

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.

This study identifies novel and known genetic contributors to hypertension using RNA-seq and eQTL analyses, highlighting potential drug targets and pathways.

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

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 paper identifies INKILN, a human-specific lncRNA that promotes vascular smooth muscle inflammation by stabilizing MKL1 and interacting with USP10.

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.