Kenneth C Bedi

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 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.

The paper integrates single-cell and spatial multiomic data to show widespread reactivation of developmental programs in diseased human hearts, with insights into transcriptional factors and localized fetal reactivation.

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 examines changes in organelle apposition in human heart failure cardiomyocytes, finding increased distances between mitochondria and sarcoplasmic reticulum/lipid droplets, along with altered molecular tethers.

This study shows that DSP haploinsufficiency causes cell-cell adhesion failure in cardiomyopathy and that increasing DSP expression rescues this defect.

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.

The paper investigates how the tubulin code is rewritten during cardiac hypertrophy and failure through transcriptional, autoregulatory, and post-translational mechanisms.

The paper uses single-nucleus RNA sequencing to define the transcriptional and cellular diversity of the non-failing human heart, identifying 9 major cell types and 20 subclusters.