| Literature DB >> 30846611 |
Kentaro Hirose1,2, Alexander Y Payumo1,2, Stephen Cutie1,2, Alison Hoang1,2, Hao Zhang3, Romain Guyot4, Dominic Lunn1,2, Rachel B Bigley1,2, Hongyao Yu5, Jiajia Wang5, Megan Smith6, Ellen Gillett7, Sandra E Muroy8, Tobias Schmid9, Emily Wilson3, Kenneth A Field10, DeeAnn M Reeder10, Malcom Maden11, Michael M Yartsev9, Michael J Wolfgang12, Frank Grützner7, Thomas S Scanlan13, Luke I Szweda14, Rochelle Buffenstein6, Guang Hu5, Frederic Flamant4, Jeffrey E Olgin1,3, Guo N Huang15,2.
Abstract
Tissue regenerative potential displays striking divergence across phylogeny and ontogeny, but the underlying mechanisms remain enigmatic. Loss of mammalian cardiac regenerative potential correlates with cardiomyocyte cell-cycle arrest and polyploidization as well as the development of postnatal endothermy. We reveal that diploid cardiomyocyte abundance across 41 species conforms to Kleiber's law-the ¾-power law scaling of metabolism with bodyweight-and inversely correlates with standard metabolic rate, body temperature, and serum thyroxine level. Inactivation of thyroid hormone signaling reduces mouse cardiomyocyte polyploidization, delays cell-cycle exit, and retains cardiac regenerative potential in adults. Conversely, exogenous thyroid hormones inhibit zebrafish heart regeneration. Thus, our findings suggest that loss of heart regenerative capacity in adult mammals is triggered by increasing thyroid hormones and may be a trade-off for the acquisition of endothermy.Entities:
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Year: 2019 PMID： 30846611 PMCID： PMC6541389 DOI： 10.1126/science.aar2038
Source DB: PubMed Journal: Science ISSN： 0036-8075 Impact factor: 47.728