Traci T. Goodchild

This study identifies a metabolic myopathy in HFpEF through multiomics analysis of skeletal muscle, revealing mitochondrial dysfunction and altered amino acid metabolism.

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 uses systems biology to identify mitochondrial dysfunction and metabolic disruptions as key factors in HFpEF using a rat model.