Joshua G. Travers

This study identifies T cell-derived IFNγ as a driver of ECM stiffening in HFpEF via LOXL3 in cardiac fibroblasts, showing therapeutic potential for targeting this pathway.

This study uses deuterium labeling to analyze protein turnover kinetics in hiPSCs and identifies fast-turnover proteins involved in cell division and differentiation.

The paper uses a logic-based machine learning method to predict how escitalopram reduces cardiomyocyte hypertrophy, validated through experiments and patient data.

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.