Karen A. Ocorr

This study shows that Chchd3 deficiency in Drosophila hearts impairs function through mitophagy, ROS, and ER stress, with partial rescue by antioxidant and ER stress interventions.

The paper identifies ribosomal protein genes as contributors to hypoplastic left heart syndrome through functional analysis across multiple model systems.

This paper shows rigosertib reverses hypertrophic cardiomyopathy in RAF1-associated Noonan syndrome using Drosophila, iPSC, and mouse models.

The paper identifies mitochondrial MICOS complex genes, CHCHD3 and CHCHD6, as contributors to hypoplastic left heart syndrome through functional studies in Drosophila and genetic analysis of patient cohorts.

The paper identifies genetic networks and regulatory elements associated with cardiac performance variation in Drosophila and finds conserved genetic architecture between flies and humans.

The paper investigates the role of KCa1.1 in sinus node function and arrhythmia risk across species, finding conserved effects of its loss of function.

The paper creates a single-cell atlas of the Drosophila embryonic heart and identifies Tinman's cell-type-specific roles in cardiac development.

The paper identifies LRP2 as a novel genetic driver of hypoplastic left heart syndrome using whole genome sequencing and multi-model systems.

This study identifies fstl1b as critical for cardiac development in zebrafish, showing its role in regulating sarcomere structure and contractility through modulation of BMP signaling.

This study shows activin signaling negatively regulates cardiac autophagy and health during aging in Drosophila, with mTORC2 playing a key role.