Anthony J. Baker, Ph.D. has a longstanding interest in the cellular and molecular mechanisms that regulate cardiac muscle contraction in health and disease. We use multiple approaches to monitor cardiac function in experimental preparations that span a range of complexity from contraction of myofilaments in-vitro, intact single cells, electrically stimulated intact cardiac muscle, intact hearts in-vitro, and intact hearts in-vivo. A major goal is to investigate new therapies to treat heart failure.
Heart failure is a leading cause of death and disability and new therapies are needed to treat this devastating disease. Research in the Baker lab focuses on both of the major pumping chambers of the heart, the left ventricle (LV) and right ventricle (RV).
We are investigating the mechanisms causing failure of the LV subsequent to a heart attack, where blood flow stops to a region of the heart resulting in death of muscle cells in that region, termed a myocardial infarction (MI). We are studying the weakened border-zone immediately adjacent to the MI. We are investigating the mechanisms that cause gradual enlargement of this weakened border-zone, ultimately leading to dilation of the heart and LV failure. We are investigating treatments to stabilize the border-zone to slow or halt the progression to heart failure after MI.
We are also investigating the mechanisms involved in failure of the RV. RV failure is relatively understudied and poorly understood. It has been assumed that an understanding of RV failure can be extrapolated from studies of LV failure. In contrast, we have found that the RV has distinctive properties compared to the LV, and the regulation of RV contraction in heart failure differs compared to the failing LV, suggesting that treatment strategies for the failing RV should be tailored to the distinctive biology of the RV.