Stavros George Drakos

This study shows that lactate can be directly imported into mitochondria and oxidized to support cardiac energy production, independent of the pyruvate carrier.

This paper integrates clinical and transcriptomic data to identify LRRN4CL as a predictor of myocardial recovery in heart failure patients undergoing LVAD therapy, showing its association with cardiomyocyte dysfunction.

This study identifies EFHD1 as a Ca2+-dependent stabilizer of ER-mitochondrial contacts that drives liver injury in MASH by promoting mitochondrial fragmentation and antiviral stress responses.

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 identifies DNA methylation and gene expression changes in heart failure patients before and after LVAD therapy, linking extracellular matrix and cytoskeletal remodeling to myocardial recovery.

This study identifies RUNX1 as a key regulator of cardiac recovery by reprogramming macrophages, showing that its inhibition promotes heart function recovery in a chronic heart failure model.

The paper integrates single-cell multi-omics and 3D genome data from human hearts to identify gene regulatory changes and causal genetic contributors in heart failure.

This study shows that cardiomyocyte renewal is significantly reduced in end-stage heart failure but increases in patients with improved cardiac function from left ventricle support devices.

This study shows that inhibiting MCT4 to redirect pyruvate metabolism reduces myocardial ischemia-reperfusion injury by improving mitochondrial function and reducing oxidative stress.

This study integrates clinical and transcriptomic data to predict myocardial recovery in heart failure patients after LVAD implantation, identifying 80 features with an AUC of 0.731.

The paper identifies a large, non-selective ionic current in mitochondria, called LUNA, which increases during cardiac injury and is inhibited by amiloride.

The paper defines the cellular and transcriptional features of cardiac recovery using snRNA-seq, identifying RUNX1 downregulation as a key predictor and potential therapeutic target.