Thomas M. Vondriska

The paper shows that collagen abundance alone does not define fibrosis in DMD, as distinct matrix states with different biological activities and mechanosignaling exist.

This study shows that increased CPT1a expression protects the heart from pathological stress by suppressing harmful gene programs, and gene transfer can rescue cardiac function in disease models.

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 study identifies dysregulated nitrosylation dynamics in HFpEF patients and ZSF1 obese rats, showing elevated nitrosative stress markers and impaired trans- and de-nitrosylase activity.

This study shows H2S deficiency in HFpEF patients and models, and that H2S supplementation or combination with GLP-1/glucagon agonists improves HFpEF outcomes.

The paper develops an algorithm to correct cell-type composition in bulk RNAseq data, revealing novel gene pathways in post-myocardial infarction cardiac remodeling.

This study shows that phenylephrine induces rapid fibrotic remodeling and ventricular dysfunction in mice through myocyte and fibroblast transcriptome reprogramming.

This study shows Bmal1 is essential for neonatal myocyte growth, histone turnover, and chromatin organization, with Sik1 as a novel clock-controlled gene linking myocyte growth to gene transcription.

The paper identifies decreased FGF13 expression in left atrial cardiomyocytes as a factor increasing vulnerability to postoperative atrial fibrillation in humans.

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