Zoltan Pierre Arany

This study identifies ROR2 as a driver of right ventricular failure by disrupting proteostasis, showing that modulating ROR2 can rescue structural and functional deficits in cardiomyocytes.

This study shows that reducing hepatic ASS1 protects against obesity and liver disease by enhancing brown fat thermogenesis.

This study shows BCKDK inhibitors cause vasodilation by directly blocking the AT1R, independent of BCAA catabolism or BCKDK.

This study identifies that SGLT2 inhibitors activate pantothenate kinase 1 (PANK1) in the human heart, enhancing coenzyme-A synthesis and fuel use, which may explain their clinical benefits in heart failure.

This study identifies PDK4 as a regulator of TGF{beta}-mediated SMC contractility, showing that reducing PDK4 limits atherosclerosis by preserving SMC phenotype.

This paper develops in vivo compressed AAV-Perturb-seq to study gene knockouts in cardiomyocytes, finding mitochondrial transcriptome changes are a common response to genetic perturbation.

This study identifies CES1 deficiency as a driver of metabolic reprogramming and endothelial dysfunction in pulmonary arterial hypertension, showing its role in lipid metabolism and oxidative stress.

This study shows HIF2α prevents GLS1 clustering in mitochondria, protecting ccRCC cells from glutamine deprivation, and suggests targeting GLS1 clustering could enhance HIF2 therapy.

The paper identifies impaired AMPK signaling in AT2 cells as a driver of pulmonary fibrosis and shows restoring AMPK alleviates fibrosis in vivo.

This study shows that pancreas-specific BCKDK inhibition accelerates pancreatic cancer while systemic BCKDK inhibition reduces tumor formation.

This study shows that BT2, an inhibitor of BCKDK, reduces plasma tryptophan by displacing it from albumin, revealing an off-target effect on tryptophan metabolism.

This study identifies a nuclear branched-chain amino acid catabolism pathway in pancreatic cancer that regulates histone propionylation and gene expression.

The paper identifies sex differences in cardiac metabolism, showing female hearts have higher fatty acid oxidation gene expression and energy utilization compared to male hearts.

This study shows that SGLT2 inhibitors improve heart failure in mice independently of their metabolic effects, even when SGLT2 is absent.

This study challenges the assumption that BCAA supplementation benefits BCKDK deficiency by showing it worsens neurodevelopmental issues in a mouse model.

The paper identifies a FOG2 variant associated with coronary microvascular disease and shows it alters hypoxia-mediated gene transcription and angiogenesis.