Quinn Stanton Wells

This study examines how aging and immunosuppression affect immune cell composition and rejection risk in heart transplant recipients, finding lower rejection odds with age and specific transcriptomic changes.

This study identifies ACTN4 as a non-muscle α-actinin in cardiac sarcomeres, showing it regulates contractility, hypertrophy, and heart remodeling without disease hallmarks.

The paper integrates proteomics and transcriptomics with genetic analyses to identify molecular mechanisms and targets of coronary artery disease.

The paper identifies ZNF469 as a transcription factor regulating collagen production in liver fibrosis through computational analysis and experimental validation.

The paper develops an integrated preclinical atherosclerosis database by extracting data from mouse models and provides tools for standardized analysis and integration with transcriptomics software.

This study identifies novel genetic risk variants and potential drug targets for heart failure using GWAS and Mendelian randomization proteomics.

This study identifies genes associated with both depression and coronary artery disease that are enriched for inflammation and cardiomyopathy pathways, and finds higher prevalence of cardiomyopathy in individuals with comorbid depression-CAD.

The paper identifies pathogenic variants in arrhythmia genes in eMERGE-III participants and reclassifies variants of uncertain significance using functional studies.

This study identifies genetic risk factors for major depressive disorder and loneliness as predictors of coronary artery disease risk, particularly in women.