BIO

My name is Emily Maglin and I am currently on a pre-medical track at FSU. I have been a camp counselor for the past four years and it was through that experience that I realized my passion for working with children. Thus, I plan on becoming a pediatrician so that I may combine that passion with my love of science and providing care to others. Aside from my career aspirations, I am a part of several student organizations on campus. I am a member of the FSU Swim Club, American Medical Student Association (Pre-medical chapter at FSU), and was recently elected as a student senator for the College of Arts and Sciences. And of course, my involvement in the Undergraduate Research Opportunity Program has sparked my interest and involvement in research. Outside of the academic sphere, I love to work out, hang out with my friends, play Guitar Hero, and go to the beach!

Disease Mechanisms of Arrhythmogenic Cardiomyopathy

Abstract

Arrhythmogenic Cardiomyopathy is an inherited heart disease and a leading cause of sudden cardiac death (SCD) in the young, where exercise potentiates disease progression. ACM is brought on by mutations in genes that encoded the cardiac desmosome. Disruption of the desmosome results in myocardial inflammation, fibrotic remodeling, impaired heart contractility, and in severe cases, SCD. The current study utilized Dsg2 (mut/mut) mice, as well as age-matched wild-type (WT) mice and Dsg2 (mut/mut) mice with germline deletion of Colony Stimulating Factor-2 (Csf2-/-). Echocardiographic and ECG data were obtained from mouse hearts at 8 and 16 weeks of age after prolonged exercise exposure (via In-Cage Running Wheels with dedicated sensors for indefinite recording of distance and speed), and compared against differences in systolic function, ventricle sizes, and heart rhythm disorders [i.e., arrhythmias]. We hypothesized there will be a considerable difference in the amount of fibrotic scarring, cardiac dysfunction, and arrhythmias in Dsg2 (mut/mut) mice compared to both WT mice and Dsg2 (mut/mut;Csf2-/-) double-mutant mice after endurance running exercise. Results demonstrated that mice with homozygous mutated desmosomal genes and mice with heterozygous desmosomal genes display reduced running capacity and earlier onset of ACM. Furthermore, exercise-induced disease activation was observed in heterozygotic mice which was not previously seen in studies that used swimming as the exercise exposure.

Keywords: heart disease, ACM, mice, echocardiograms, medicine