scholarly journals Extending the time window of mammalian heart regeneration by thymosin beta 4

2014 ◽  
Vol 18 (12) ◽  
pp. 2417-2424 ◽  
Author(s):  
Liu Rui ◽  
Nie Yu ◽  
Lian Hong ◽  
He Feng ◽  
Han Chunyong ◽  
...  
Keyword(s):  
Time Window ◽  
Heart Regeneration ◽  
Thymosin Beta 4 ◽  
Mammalian Heart

scholarly journals In Vivo Activation of a Conserved MicroRNA Program Induces Mammalian Heart Regeneration

2014 ◽  
Vol 15 (6) ◽  
pp. 805
Author(s):  
Aitor Aguirre ◽  
Nuria Montserrat ◽  
Serena Zacchigna ◽  
Emmanuel Nivet ◽  
Tomoaki Hishida ◽  
...  
Keyword(s):  
Heart Regeneration ◽  
Mammalian Heart

scholarly journals Multicellular Transcriptional Analysis of Mammalian Heart Regeneration

Circulation ◽  
2017 ◽  
Vol 136 (12) ◽  
pp. 1123-1139 ◽  
Author(s):  
Gregory A. Quaife-Ryan ◽  
Choon Boon Sim ◽  
Mark Ziemann ◽  
Antony Kaspi ◽  
Haloom Rafehi ◽  
...  
Keyword(s):  
Transcriptional Analysis ◽  
Heart Regeneration ◽  
Mammalian Heart

scholarly journals In Vivo Activation of a Conserved MicroRNA Program Induces Mammalian Heart Regeneration

2014 ◽  
Vol 15 (5) ◽  
pp. 589-604 ◽  
Author(s):  
Aitor Aguirre ◽  
Nuria Montserrat ◽  
Serena Zacchigna ◽  
Emmanuel Nivet ◽  
Tomoaki Hishida ◽  
...  
Keyword(s):  
Heart Regeneration ◽  
Mammalian Heart

scholarly journals Decellularized zebrafish cardiac extracellular matrix induces mammalian heart regeneration

2016 ◽  
Vol 2 (11) ◽  
pp. e1600844 ◽  
Author(s):  
William C. W. Chen ◽  
Zhouguang Wang ◽  
Maria Azzurra Missinato ◽  
Dae Woo Park ◽  
Daniel Ward Long ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Adult Mouse ◽  
Contractile Function ◽  
Left Ventricular ◽  
Precursor Cell ◽  
Cell Populations ◽  
Mouse Heart ◽  
Heart Regeneration ◽  
Regenerative Capacity ◽  
Mammalian Heart

Heart attack is a global health problem that leads to significant morbidity, mortality, and health care burden. Adult human hearts have very limited regenerative capability after injury. However, evolutionarily primitive species generally have higher regenerative capacity than mammals. The extracellular matrix (ECM) may contribute to this difference. Mammalian cardiac ECM may not be optimally inductive for cardiac regeneration because of the fibrotic, instead of regenerative, responses in injured adult mammalian hearts. Given the high regenerative capacity of adult zebrafish hearts, we hypothesize that decellularized zebrafish cardiac ECM (zECM) made from normal or healing hearts can induce mammalian heart regeneration. Using zebrafish and mice as representative species of lower vertebrates and mammals, we show that a single administration of zECM, particularly the healing variety, enables cardiac functional recovery and regeneration of adult mouse heart tissues after acute myocardial infarction. zECM-treated groups exhibit proliferation of the remaining cardiomyocytes and multiple cardiac precursor cell populations and reactivation of ErbB2 expression in cardiomyocytes. Furthermore, zECM exhibits pro-proliferative and chemotactic effects on human cardiac precursor cell populations in vitro. These contribute to the structural preservation and correlate with significantly higher cardiac contractile function, notably less left ventricular dilatation, and substantially more elastic myocardium in zECM-treated hearts than control animals treated with saline or decellularized adult mouse cardiac ECM. Inhibition of ErbB2 activity abrogates beneficial effects of zECM administration, indicating the possible involvement of ErbB2 signaling in zECM-mediated regeneration. This study departs from conventional focuses on mammalian ECM and introduces a new approach for cardiac tissue regeneration.

ERBB2 triggers mammalian heart regeneration by promoting cardiomyocyte dedifferentiation and proliferation

2015 ◽  
Vol 17 (5) ◽  
pp. 627-638 ◽  
Author(s):  
Gabriele D’Uva ◽  
Alla Aharonov ◽  
Mattia Lauriola ◽  
David Kain ◽  
Yfat Yahalom-Ronen ◽  
...  
Keyword(s):  
Heart Regeneration ◽  
Mammalian Heart

scholarly journals Regulation of neonatal and adult mammalian heart regeneration by the miR-15 family

2012 ◽  
Vol 110 (1) ◽  
pp. 187-192 ◽  
Author(s):  
E. R. Porrello ◽  
A. I. Mahmoud ◽  
E. Simpson ◽  
B. A. Johnson ◽  
D. Grinsfelder ◽  
...  
Keyword(s):  
Heart Regeneration ◽  
Mammalian Heart

Genetic insights into mammalian heart regeneration

2017 ◽  
Vol 49 (9) ◽  
pp. 1292-1293 ◽  
Author(s):  
Ana Vujic ◽  
Vinícius Bassaneze ◽  
Richard T Lee
Keyword(s):  
Heart Regeneration ◽  
Mammalian Heart

scholarly journals Glucose metabolism promotes neonatal heart regeneration

2019 ◽  
Author(s):  
Viviana M Fajardo Martinez ◽  
Iris Feng ◽  
Bao Ying Chen ◽  
Cesar A Perez ◽  
Baochen Shi ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Glucose Transporter ◽  
Cardiac Regeneration ◽  
Glycogen Storage ◽  
Mouse Heart ◽  
Heart Regeneration ◽  
Regenerative Capacity ◽  
Metabolic Switch ◽  
Nucleotide Biosynthesis ◽  
Mammalian Heart

AbstractThe mammalian heart switches its main metabolic substrate from glucose to fatty acids shortly after birth. This metabolic switch coincides with the loss of regenerative capacity in the heart. However, it is unknown whether glucose metabolism itself regulates heart regeneration. Here, we report that glucose metabolism is a determinant of regenerative capacity in the neonatal mammalian heart. Cardiac-specific overexpression of Glut1, the embryonic form of constitutively active glucose transporter, resulted in an increase in glucose uptake and concomitant glycogen storage in postnatal heart. Upon cryoinjury, Glut1 transgenic hearts showed higher regenerative capacity with less fibrosis than non-transgenic control hearts. Interestingly, flow cytometry analysis revealed two distinct populations of ventricular cardiomyocytes: Tnnt2-high and Tnnt2-low cardiomyocytes, the latter of which showed significantly higher mitotic activity in response to high intracellular glucose in Glut1 transgenic hearts. Metabolic profiling shows that Glut1-transgenic hearts have a significant increase in the glucose metabolites upon injury, and inhibition of the nucleotide biosynthesis abrogated the regenerative advantage of high intra-cardiomyocyte glucose level. Our data suggest that the increased in glucose metabolism promotes cardiac regeneration in neonatal mouse heart.

scholarly journals GLUT1 overexpression enhances glucose metabolism and promotes neonatal heart regeneration

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Viviana M. Fajardo ◽  
Iris Feng ◽  
Bao Ying Chen ◽  
Cesar A. Perez-Ramirez ◽  
Baochen Shi ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Glucose Transporter ◽  
Cardiac Regeneration ◽  
Glycogen Storage ◽  
Mouse Heart ◽  
Heart Regeneration ◽  
Regenerative Capacity ◽  
Metabolic Switch ◽  
Nucleotide Biosynthesis ◽  
Mammalian Heart

AbstractThe mammalian heart switches its main metabolic substrate from glucose to fatty acids shortly after birth. This metabolic switch coincides with the loss of regenerative capacity in the heart. However, it is unknown whether glucose metabolism regulates heart regeneration. Here, we report that glucose metabolism is a determinant of regenerative capacity in the neonatal mammalian heart. Cardiac-specific overexpression of Glut1, the embryonic form of constitutively active glucose transporter, resulted in an increase in glucose uptake and concomitant accumulation of glycogen storage in postnatal heart. Upon cryoinjury, Glut1 transgenic hearts showed higher regenerative capacity with less fibrosis than non-transgenic control hearts. Interestingly, flow cytometry analysis revealed two distinct populations of ventricular cardiomyocytes: Tnnt2-high and Tnnt2-low cardiomyocytes, the latter of which showed significantly higher mitotic activity in response to high intracellular glucose in Glut1 transgenic hearts. Metabolic profiling shows that Glut1-transgenic hearts have a significant increase in the glucose metabolites including nucleotides upon injury. Inhibition of the nucleotide biosynthesis abrogated the regenerative advantage of high intra-cardiomyocyte glucose level, suggesting that the glucose enhances the cardiomyocyte regeneration through the supply of nucleotides. Our data suggest that the increase in glucose metabolism promotes cardiac regeneration in neonatal mouse heart.

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