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Times Cited: 361
Times Cited
Times Co-cited
Similarity
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Enzo R Porrello, Ahmed I Mahmoud, Emma Simpson, Joseph A Hill, James A Richardson, Eric N Olson, Hesham A Sadek. Science 2011
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Hypoxia induces heart regeneration in adult mice.
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ERBB2 triggers mammalian heart regeneration by promoting cardiomyocyte dedifferentiation and proliferation.
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The oxygen-rich postnatal environment induces cardiomyocyte cell-cycle arrest through DNA damage response.
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Regulation of neonatal and adult mammalian heart regeneration by the miR-15 family.
Enzo R Porrello, Ahmed I Mahmoud, Emma Simpson, Brett A Johnson, David Grinsfelder, Diana Canseco, Pradeep P Mammen, Beverly A Rothermel, Eric N Olson, Hesham A Sadek. Proc Natl Acad Sci U S A 2013
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Functional screening identifies miRNAs inducing cardiac regeneration.
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Mammalian heart renewal by pre-existing cardiomyocytes.
Samuel E Senyo, Matthew L Steinhauser, Christie L Pizzimenti, Vicky K Yang, Lei Cai, Mei Wang, Ting-Di Wu, Jean-Luc Guerquin-Kern, Claude P Lechene, Richard T Lee. Nature 2013
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The extracellular matrix protein agrin promotes heart regeneration in mice.
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Hippo pathway effector Yap promotes cardiac regeneration.
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Neuregulin1/ErbB4 signaling induces cardiomyocyte proliferation and repair of heart injury.
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Hypoxia fate mapping identifies cycling cardiomyocytes in the adult heart.
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Hippo pathway inhibits Wnt signaling to restrain cardiomyocyte proliferation and heart size.
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Evidence for hormonal control of heart regenerative capacity during endothermy acquisition.
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Zebrafish heart regeneration occurs by cardiomyocyte dedifferentiation and proliferation.
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A microRNA-Hippo pathway that promotes cardiomyocyte proliferation and cardiac regeneration in mice.
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Frequency of mononuclear diploid cardiomyocytes underlies natural variation in heart regeneration.
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YAP1, the nuclear target of Hippo signaling, stimulates heart growth through cardiomyocyte proliferation but not hypertrophy.
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MicroRNA therapy stimulates uncontrolled cardiac repair after myocardial infarction in pigs.
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Pitx2 promotes heart repair by activating the antioxidant response after cardiac injury.
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Cyclin A2 induces cardiac regeneration after myocardial infarction through cytokinesis of adult cardiomyocytes.
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Functional Recovery of a Human Neonatal Heart After Severe Myocardial Infarction.
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Overexpression of Tbx20 in Adult Cardiomyocytes Promotes Proliferation and Improves Cardiac Function After Myocardial Infarction.
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Cardiomyocyte proliferation contributes to heart growth in young humans.
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p38 MAP kinase inhibition enables proliferation of adult mammalian cardiomyocytes.
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Epicardial FSTL1 reconstitution regenerates the adult mammalian heart.
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Primary contribution to zebrafish heart regeneration by gata4(+) cardiomyocytes.
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Loss of microRNA-128 promotes cardiomyocyte proliferation and heart regeneration.
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Macrophages are required for neonatal heart regeneration.
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A calcineurin-Hoxb13 axis regulates growth mode of mammalian cardiomyocytes.
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Existing cardiomyocytes generate cardiomyocytes at a low rate after birth in mice.
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Human embryonic-stem-cell-derived cardiomyocytes regenerate non-human primate hearts.
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mir-17-92 cluster is required for and sufficient to induce cardiomyocyte proliferation in postnatal and adult hearts.
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MiR-15 family regulates postnatal mitotic arrest of cardiomyocytes.
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Cyclin A2 mediates cardiomyocyte mitosis in the postmitotic myocardium.
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Nrg1 is an injury-induced cardiomyocyte mitogen for the endogenous heart regeneration program in zebrafish.
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Single-cell analysis uncovers that metabolic reprogramming by ErbB2 signaling is essential for cardiomyocyte proliferation in the regenerating heart.
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c-kit+ cells minimally contribute cardiomyocytes to the heart.
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FGF1/p38 MAP kinase inhibitor therapy induces cardiomyocyte mitosis, reduces scarring, and rescues function after myocardial infarction.
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Co-cited is the co-citation frequency, indicating how many articles cite the article together with the query article. Similarity is the co-citation as percentage of the times cited of the query article or the article in the search results, whichever is the lowest. These numbers are calculated for the last 100 citations when articles are cited more than 100 times.