Saptarsi M. Haldar

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 SGLT2 inhibitors improve heart failure in mice independently of their metabolic effects, even when SGLT2 is absent.

This study identifies PDGFD as a CAD risk gene, showing it promotes SMC expansion, migration, and inflammation, contributing to vascular calcification and plaque recruitment.

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 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.

The paper investigates the role of developmentally regulated cardiac lincRNAs in heart development and function, finding that their deletion does not cause severe cardiac phenotypes.

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.