Kory J. Lavine

This study shows that blocking CD14 reduces arrhythmogenic cardiomyopathy in mice by decreasing inflammation and fibrosis.

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

The paper identifies multicellular molecular programs associated with RV adaptation in PAH using single-nucleus RNA sequencing and integrates them with physiological measurements.

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.

The paper identifies stress granule coarsening as a critical factor in cardiac electrophysiological dysfunction under oxidative stress.

Human arrhythmogenic cardiomyopathy hearts harbor a lesion niche of POSTN fibroblasts and NLRP3+ inflammatory macrophages; IL-1β neutralization in Dsg2-mutant mice reduced fibrosis, dysfunction, and ventricular ectopy.

This paper integrates clinical and transcriptomic data to identify LRRN4CL as a predictor of myocardial recovery in heart failure patients undergoing LVAD therapy, showing its association with cardiomyocyte dysfunction.

This study shows that the aged muscle tissue environment limits muscle stem cell function, and combined interventions can partially restore muscle mass in aged mice.

This study identifies circulating miRNA and protein signatures that predict clinical outcomes in pediatric dilated cardiomyopathy with high discriminatory accuracy.

This study uses spatial transcriptomics to show that myocarditis involves widespread molecular changes in cardiomyocytes, not just immune cell areas.

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

Single-cell and spatial maps of human coronary arteries identify FAP as a marker of SMC-derived modulated cells; an anti-FAP BiTE reduced plaque burden in mouse models.

The paper introduces an unbiased proteomic platform for ATE1-based arginylation profiling, identifying 235 unique arginylation sites in human proteomes.

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.

The paper identifies macrophage-like vascular smooth muscle cells as dominant in early atherosclerosis and shows that targeting iron regulation inhibits their transition.

This study identifies the secretome of cardiac fibroblasts in healthy and infarcted mouse hearts, revealing dynamic paracrine factors and potential biomarkers or therapeutic targets.

This study shows CD40 agonists promote myocardial inflammation by activating CCR2+ macrophages and CD8 T-cells, leading to heart failure.

The paper identifies two distinct pathways for replenishing resident peritoneal macrophages after injury, with differing reliance on monocytes and intermediate stages.

This study shows that inhibiting soluble epoxide hydrolase reduces inflammation and myocardial injury in arrhythmogenic cardiomyopathy by increasing pro-resolving lipid mediators.

This paper links CAD GWAS variants to causal genes in SMCs using single-cell chromatin accessibility and Hi-C data, creating a scV2E2G map for disease mechanism discovery.

This study shows that the ACTA1 R256H mutation disrupts actin structure and function in cardiomyocytes, leading to reduced contractility and a likely causative role in dilated cardiomyopathy.

The paper identifies causal genes in heart disease GWAS loci by integrating Hi-C, chromatin accessibility, and transcriptomic data, revealing regulatory relationships in cardiac fibroblasts.

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 integrates clinical and transcriptomic data to predict myocardial recovery in heart failure patients after LVAD implantation, identifying 80 features with an AUC of 0.731.

This study connects genotype, phenotype, and drug response in dilated cardiomyopathy using molecular mechanism-based computational and experimental approaches for a troponin T mutation.

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 generates a high-resolution spatial multi-omic map of human myocardial infarction by integrating single-cell gene expression, chromatin accessibility, and spatial transcriptomic data to reveal cellular zones of injury, repair, and remodeling.

This study uses single cell transcriptomics to analyze heart failure in humans, identifying cell type-specific transcriptional changes and disease-associated states.

This study identifies SVEP1 as a novel coronary artery disease locus that promotes atherosclerosis by affecting vascular smooth muscle cell function and signaling pathways.