Dynamic reciprocity between cells and the extracellular environment in heart disease
Department
Biological Sciences
Document Type
Poster
Start Date
2-26-2025 3:00 PM
End Date
2-26-2025 5:00 PM
Abstract
Many heart diseases result in the accumulation of scar tissue known as cardiac fibrosis. In response to an injury whether that be a myocardial infarction, hypertension, or a genetic heart disease, the cardiac tissue generates fibrotic scar tissue to replace damaged heart tissue that is composed of extracellular matrix proteins. This response is necessary to maintain cardiac function but, overtime, the scar tissue creates a pathological environment that can diminish cardiac function and lead to heart failure. In our lab, we study this process in the context of Duchenne muscular dystrophy, the most common fatal genetic disease in children in which the majority of patients develop cardiomyopathy and heart failure. Using a mouse model of this disease, we isolate cardiac tissue and study two prominent cell types, fibroblasts and macrophages, that are responsible for the fibrotic response. Using cell culture and microscopy techniques, we are able to measure the interaction between the scar tissue and the cells and use this platform to identify targets for therapeutic intervention.
Recommended Citation
Towner, Jackie; Puumala, Eric; Knapp, Callie; Larsen, Kjersten; and Falgetelli, Natalia, "Dynamic reciprocity between cells and the extracellular environment in heart disease" (2025). Day of Scholarship. 7.
https://spark.bethel.edu/dayofscholarship/spring2025/feb26/7
Dynamic reciprocity between cells and the extracellular environment in heart disease
Many heart diseases result in the accumulation of scar tissue known as cardiac fibrosis. In response to an injury whether that be a myocardial infarction, hypertension, or a genetic heart disease, the cardiac tissue generates fibrotic scar tissue to replace damaged heart tissue that is composed of extracellular matrix proteins. This response is necessary to maintain cardiac function but, overtime, the scar tissue creates a pathological environment that can diminish cardiac function and lead to heart failure. In our lab, we study this process in the context of Duchenne muscular dystrophy, the most common fatal genetic disease in children in which the majority of patients develop cardiomyopathy and heart failure. Using a mouse model of this disease, we isolate cardiac tissue and study two prominent cell types, fibroblasts and macrophages, that are responsible for the fibrotic response. Using cell culture and microscopy techniques, we are able to measure the interaction between the scar tissue and the cells and use this platform to identify targets for therapeutic intervention.
