Janet R. Manning

This study shows that Trf2 is critical for cardiac development and function, with CM-specific loss causing heart morphology defects and cardiac dysfunction without telomere shortening.

This study shows that GCN5L1 loss increases pyruvate dehydrogenase phosphorylation, inhibiting glucose oxidation and worsening myocardial damage during ischemia-reperfusion injury.

This study shows Adropin treatment reverses cardiac dysfunction and metabolic defects in a mouse model of HFpEF by reducing O-GlcNAcylation of LCAD and improving fatty acid oxidation.

This study identifies Gcn5l1 as a heart-specific factor that modulates cholesterol metabolism and heart-to-liver crosstalk in cardiometabolic heart failure, revealing the heart's role in systemic metabolic dysfunction.

This study shows that TCA cycle dysfunction and amino acid catabolism in mice with HFpEF drive hepatic steatosis similar to human NAFLD.

This study shows GCN5L1 prevents Rictor degradation in cardiac cells under hypoxia by acetylating Rictor, thereby maintaining Akt/mTORC2 signaling and protecting against ischemic injury.