Junedh Amrute

The paper identifies a compact regulatory logic governing fibroblast plasticity in fibrosis by analyzing enhancer repression and gene perturbations across multiple tissues.

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

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 maps monocyte differentiation trajectories in the infarcted heart using genetic lineage tracing and single-cell RNA-sequencing, identifying a protective IFN-responsive macrophage subset.

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 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.

This study shows that LPS pretreatment protects hearts from ISO-induced injury through TLR4-mediated interferon signaling, involving both cell-autonomous and non-cell-autonomous mechanisms.

The paper identifies causal genetic mechanisms at CAD GWAS loci using CRISPR screens and chromatin analysis, revealing enhancer-gene links and ancestry/sex-specific risk factors.

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 bZIP transcription factors as key regulators of IL-2-induced Treg activation, linking chromatin accessibility changes to Th1/Th2 molecular phenotypes and metabolic pathways.

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.

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.

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.