Timothy A. McKinsey

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 SPLAT-TR to analyze proteome changes in ER stress, revealing distinct temporal phases of protein translocation, clearance, and degradation in different organelles.

This study shows low-dose GLP-1RA therapy improves cardiac and hepatic function in HFpEF without weight loss, through mechanisms like reduced fibrosis and lipid accumulation.

This paper shows that β1- and β2-adrenergic receptor haplotypes influence responses to bucindolol and placebo in heart failure patients, with internalizing haplotypes providing protection and bucindolol being effective in internalization-resistant ones.

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.

This study shows that inhibiting HDAC11 in adipocytes increases UCP1 expression and thermogenesis, even when beta-AR signaling is blocked.

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

This study shows that HDAC11 suppresses thermogenic programs in adipose tissue via BRD2, leading to improved metabolic outcomes in HDAC11-deficient mice.