Michael Alexanian

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

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 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 uses single-cell multimodal analyses to show how maternal diabetes alters epigenomic and transcriptomic states in cardiac and craniofacial progenitors, leading to developmental defects.

The paper identifies BRD4-dependent immune-fibroblast crosstalk via IL1B in heart failure, showing IL1B inhibition reduces fibroblast activation and improves cardiac function.

The paper uses single-cell epigenomics and machine learning to model cell-cell communication networks in cardiac development and identify dysregulation in TBX1 deletion.

The paper identifies a reversible transcriptional switch in cardiac fibroblasts that governs fibroblast plasticity and contributes to chronic heart disease, with MEOX1 as a key regulator.

This study identifies a BRD4-GATA4 interaction that regulates mitochondrial homeostasis in adult cardiomyocytes by modulating gene expression related to energy production.

This study shows that human iPSC-derived organoids can model the cooperative development of cardiac and gut tissues through paracrine signaling.

This study shows BRD4 promotes cardiac fibrosis by dynamically targeting chromatin and activating gene expression in fibroblasts, revealing a signaling pathway involved in heart failure.