Investigating the role of protein CCN3 in the heart
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Heart failure is the number one cause of death in both men and women in the state of Wisconsin. African Americans and Native Americans are disproportionately affected by heart failure compared to White, Asian, and Hispanic counterparts in Wisconsin. Considering the vast proportion of the population that is affected by heart failure, there is a pressing need to understand the mechanisms by which heart failure occurs so that new therapeutic strategies can be developed for treating this disease.
More than half of heart failure cases in Wisconsin are categorized as ischemic heart failure, which means that heart failure develops as a result of a heart attack. During a heart attack, vessels that deliver oxygenated blood to the cardiac tissue become blocked causing damage and cellular death to the infarcted region. The typical ischemic injury response consists of overactivation of scar producing cells which causes stiffening of the heart wall and can lead to progressive heart failure. While most patients survive the initial heart attack, there are surprisingly few therapeutic strategies for treating heart failure progression, and ever fewer strategies for treating progressive cardiac scarring.
After a heart attack, scar producing cells called myofibroblasts play an important role in preventing the damaged heart wall from catastrophic rupture, which would certainly result in immediate death. However, prolonged activation of cardiac myofibroblasts long after the initial ischemic event can contribute to excessive scar production contributing to heart failure progression. An overarching goal of the researcher’s lab is to understand the cellular and molecular processes contributing to heart failure so that they can develop therapeutic strategies to improve outcomes post heart attack. In preliminary studies the research team found that a protein called CCN3, which is produced by cardiac myofibroblasts after heart attack, appears to contribute to excessive cardiac scarring and heart failure. The goal of the proposed study is to test the cellular and physiological consequences of inhibiting or overexpressing CCN3 in cardiac myofibroblasts following heart attack. The team further proposes to investigate how CCN3 signals to various cardiac cell types to cause cell dysfunction.
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