David A. Kass

This paper shows that loss of PFKFB2 in cardiac cells leads to electrophysiological instability, including prolonged repolarization and ventricular tachyarrhythmia, linking glycolytic regulation to heart function.

The paper identifies multicellular molecular programs associated with RV adaptation in PAH using single-nucleus RNA sequencing and integrates them with physiological measurements.

This study shows that reduced myocardial serine synthesis impairs cardiac stress responses by disrupting redox balance, one-carbon metabolism, and amino acid homeostasis.

This study identifies two distinct cardiac proteomic signatures in HFpEF linked to sex ratios, revealing molecular differences in structural machinery and cellular communication.

This study identifies nuclear GAPDH translocation as a mediator of stress-induced cardiac hypertrophy through BRG1-associated chromatin remodeling in mice and human patients.

This study shows that DSG2 deficiency causes cardiac dysfunction by impairing Z-disc and intercalated disc mechanotransduction, leading to structural and functional cardiac defects.

The paper identifies unique proteomic changes in ATTR-CM hearts, showing upregulated endocytosis and downregulated sarcomere proteins compared to controls.

The paper uses random survival forests to identify 33 myocardial genes predictive of survival in HFpEF, outperforming clinical parameters in prognosis modeling.

This study shows that macrophages with constitutive mTORC1 activation via TSC2 deletion reduce inflammation and improve cardiac function after ischemia-reperfusion injury by increasing GPNMB expression.

This paper uses snRNA-seq to analyze human HFpEF myocardium, identifying differential gene expression and pathway enrichment in cardiomyocytes and fibroblasts compared to controls and DCM.

This study investigates the role of ATP citrate lyase (ACLY) in cardiac function and NAD+/NADH balance, finding it is reduced in heart failure and its inhibition impairs cardiac function and metabolism.

This study identifies PGC1/PPAR signaling and its regulators Yap1 and SF3B2 as key drivers of cardiomyocyte maturation through single-cell transcriptomic analysis across neonatal to adult hearts.

This study shows that myocardial BDNF signaling via YY1 regulates cardiac bioenergetics and mitochondrial function during stress.

The paper integrates proteomic and genomic data from skeletal muscle myocytes to identify gene and protein expression differences between slow and fast-twitch fiber types.