Leslie Anne Leinwand

This study investigates cardiac myofibril remodeling in Burmese pythons during digestion using multi-omics approaches, revealing post-translational modifications as key to increased contractility.

The paper identifies a conserved postprandial metabolite, pTOS, that links nutrient intake to energy balance through a gut-brain pathway in pythons and mice, with potential relevance to humans.

This study compares the progression of skeletal muscle atrophy caused by fasting and disuse across different muscle fiber types using transcriptomic analysis.

The paper assembles and annotates the first whole genome of the ball python (Python regius), providing a high-quality resource for studying snake-specific traits and physiological adaptations.

This study shows that Burmese pythons can sustain cardiac growth through cardiomyocyte hyperplasia by re-entering the cell cycle after frequent feeding.

The paper identifies CaMKIIδ-B subcellular localization as a determinant of myocardial recovery in heart failure, showing cytoplasmic retention impairs recovery.

This study examines age-dependent differences in cardiac hypertrophy and regression in female mice following exercise and detraining, identifying distinct molecular pathways in young versus adult hearts.

This study identifies FoxO1-dependent autophagy as a conserved mechanism for regression of physiological cardiac hypertrophy across species.

This paper introduces a DLP-based 3D printing method for rapid, high-efficiency fabrication of human engineered heart tissues to model cardiac disease.

The paper identifies lncMYH7b as a regulatory long noncoding RNA in the human heart that influences the ratio of β-MyHC to α-MyHC through TEAD1/TEAD3 regulation, independent of miR-499.

This study shows miR-206 is necessary for maintaining a slow muscle phenotype in both skeletal and cardiac muscle and contributes to sexual dimorphisms.

This paper describes a mouse model of Laing distal myopathy caused by the R1500P mutation in {beta}-myosin, showing structural and functional muscle defects and weakened acto-myosin binding.

This study investigates sex differences and stimulus-specific mechanisms in the regression of pathological cardiac hypertrophy in mouse models.