Dr. Molkentin’s research program continues to focus on cardiovascular and skeletal muscle disease through examination of basic signaling mechanisms. His larger projects include defining the molecular mechanisms that underlie cell death, with a special interest in mitochondrial-dependent mechanisms of non-apoptotic death. The laboratory is also interested in characterizing the intracellular signaling pathways that control cellular growth, differentiation, and replication in cardiac and skeletal muscle. For example, the laboratory has a strong track record of publications detailing the intracellular signaling effectors (kinases and phosphatases) that underlie the cardiac hypertrophic response or the transition of the heart into dilated failure, as well as the disease response of dystrophic skeletal muscle. His laboratory is also actively engaged in identifying novel secreted protein factors (cytokines, growth factors, chemokines, etc) from the heart and skeletal muscle that might control disease responsiveness. His laboratory is also actively engaged in studying the cardiac and skeletal muscle fibroblast and how it functions during disease to alter the extracellular matrix, which impacts tissue remodeling. More recently his laboratory has been investigating the cellular mechanisms underlying cardiac repair, either by regulating cell cycle in cardiomyocytes or interrogating the role of putative cardiac progenitor cells. Finally, his laboratory continues to investigate basic mechanisms of intracellular calcium handling in cardiac and skeletal muscle to further explore the paradigms of excitation-transcription coupling and excitation-signaling coupling. Publications covering these project areas span high impact journals such as Cell, Science, Nature, and Nature Medicine.
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