Recent advances raise the possibility of therapies that limit damage to heart muscle during heart attack or that enable tissue regeneration after heart attack and other trauma, but there is much more to be learned. Scientists in this area study the signaling mechanisms and machinery that regulate how the heart muscle responds to and protects itself from ischemia (inadequate blood flow); the contraction, relaxation, and remodeling of the heart; and the mechanisms that instruct cells to form myocytes and build a heart.

Heart muscle denied blood flow for short periods is relatively protected from subsequent periods of inadequate blood supply. Cell biologists working to identify the molecules and signaling pathways that underlie this phenomenon work with animal modelers to test hypotheses regarding the mechanisms involved. Recent studies have shown that heart failure after damage is in part due to deranged calcium signaling, the signal for cell contraction, in heart muscle cells. Scientists are also uncovering the exact mechanisms by which such signaling is impaired and developing means of correcting it. Collaboration with molecular imaging experts and physicians working to help patients with ischemic heart disease or heart failure will develop techniques to follow the activation of protective pathways and “normalization” of the contraction signaling pathways to aid translation of finding in the laboratory to patients.

Cell and developmental biologists are now studying the signaling mechanisms that trigger the formation, growth, and death of heart muscle cells and that regulate remodeling of the heart, and collaborations with physician-scientists developing treatments for patients with inherited and acquired diseases of the heart muscle are beginning.