John Travis Hinson, MD

My laboratory utilizes genomic approaches to interrogate mechanisms of inherited cardiovascular disorders especially those that lead to heart failure. We are particularly interested in developing single cell and cardiac microtissue assays derived from disease-specific, human induced pluripotent stem cells (iPScs) in combination with in vivo mouse models. My lab's current research focus is directed toward: 1) defining the role of AMPactivated protein kinase in physiologic and pathologic forms of cardiac remodeling; 2) engineering cardiac microtissues to study the most common forms of familial hypertrophic and dilated cardiomyopathies due to sarcomere mutations; and 3) to develop assays for high-throughput functional genomic screens to predict pathogenicity of genetic variation in cardiomyopathy genes. These studies capitalize on the laboratory's expertise in human genetics, stem cell biology, tissue engineering and computational methods.

[2026] Advancing gene and base editing for cardiovascular disease: overcoming barriers in delivery, precision and safety. [2025] Phenotype specific nuclear lamina remodeling in hiPSC derived cardiomyocytes bearing TNNT2 sarcomeric variants. [2024] Adducin Regulates Sarcomere Disassembly During Cardiomyocyte Mitosis. [2024] CRISPR Activation Reverses Haploinsufficiency and Functional Deficits Caused by TTN Truncation Variants. [2024] TTN truncation variants produce sarcomere-integrating proteins of uncertain functional significance. [2023] Metabolic fitness of IgA+ plasma cells in the gut requires DOCK8.