Daniel W Sorensen1,2,3, Jop H van Berlo4,5,6,7. 1. Lillehei Heart Institute, Department of Medicine, University of Minnesota, Minneapolis, MN, USA. 2. Department of Genetics, Cell Biology, and Development, University of Minnesota, Minneapolis, MN, USA. 3. Stem Cell Institute, University of Minnesota, Minneapolis, MN, USA. 4. Lillehei Heart Institute, Department of Medicine, University of Minnesota, Minneapolis, MN, USA. jvanberl@umn.edu. 5. Stem Cell Institute, University of Minnesota, Minneapolis, MN, USA. jvanberl@umn.edu. 6. Integrative Biology and Physiology graduate program, University of Minnesota, Minneapolis, MN, USA. jvanberl@umn.edu. 7. Cancer and Cardiovascular Research Building, University of Minnesota, 2231 6th St SE, Minneapolis, MN, 55455, USA. jvanberl@umn.edu.
Abstract
PURPOSE OF REVIEW: The loss of contractile function after heart injury remains one of the major healthcare issues of our time. One strategy to deal with this problem would be to increase the number of cardiomyocytes to enhance cardiac function. In the last couple of years, reactivation of cardiomyocyte proliferation has repeatedly demonstrated to aid in functional recovery after cardiac injury. RECENT FINDINGS: The Tgf-β superfamily plays key roles during development of the heart and populating the embryonic heart with cardiomyocytes. In this review, we discuss the role of Tgf-β signaling in regulating cardiomyocyte proliferation during development and in the setting of cardiac regeneration. Although various pathways to induce cardiomyocyte proliferation have been established, the extent to which cardiomyocyte proliferation requires or involves activation of the Tgf-β superfamily is not entirely clear. More research is needed to better understand cross-talk between pathways that regulate cardiomyocyte proliferation.
PURPOSE OF REVIEW: The loss of contractile function after heart injury remains one of the major healthcare issues of our time. One strategy to deal with this problem would be to increase the number of cardiomyocytes to enhance cardiac function. In the last couple of years, reactivation of cardiomyocyte proliferation has repeatedly demonstrated to aid in functional recovery after cardiac injury. RECENT FINDINGS: The Tgf-β superfamily plays key roles during development of the heart and populating the embryonic heart with cardiomyocytes. In this review, we discuss the role of Tgf-β signaling in regulating cardiomyocyte proliferation during development and in the setting of cardiac regeneration. Although various pathways to induce cardiomyocyte proliferation have been established, the extent to which cardiomyocyte proliferation requires or involves activation of the Tgf-β superfamily is not entirely clear. More research is needed to better understand cross-talk between pathways that regulate cardiomyocyte proliferation.
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