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The DOI matches its Crossref record; 13 of the 13 references it cites were found in a registry or an index.

The Oxygen-Rich Postnatal Environment Induces Cardiomyocyte Cell-Cycle Arrest through DNA Damage Response

Open access
Puente, Bao N., Kimura, Wataru, Muralidhar, Shalini A., Moon, Jesung, Amatruda, James F., Phelps, Kate L., Grinsfelder, David, Rothermel, Beverly A., Chen, Rui, Garcia, Joseph A., Santos, Celio X., Thet, SuWannee, Mori, Eiichiro, Kinter, Michael T., Rindler, Paul M., Zacchigna, Serena, Mukherjee, Shibani, Chen, David J., Mahmoud, Ahmed I., Giacca, Mauro, Rabinovitch, Peter S., Asaithamby, Aroumougame, Shah, Ajay M., Szweda, Luke I., Sadek, Hesham A.·2014·Cell
DOI 10.1016/j.cell.2014.03.032
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Abstract

Summary The mammalian heart has a remarkable regenerative capacity for a short period of time after birth, after which the majority of cardiomyocytes permanently exit cell cycle. We sought to determine the primary post-natal event that results in cardiomyocyte cell-cycle arrest. We hypothesized that transition to the oxygen rich postnatal environment is the upstream signal that results in cell cycle arrest of cardiomyocytes. Here we show that reactive oxygen species (ROS), oxidative DNA damage, and DNA damage response (DDR) markers significantly increase in the heart during the first postnatal week. Intriguingly, postnatal hypoxemia, ROS scavenging, or inhibition of DDR all prolong the postnatal proliferative window of cardiomyocytes, while hyperoxemia and ROS generators shorten it. These findings uncover a previously unrecognized protective mechanism that mediates cardiomyocyte cell cycle arrest in exchange for utilization of oxygen dependent aerobic metabolism. Reduction of mitochondrial-dependent oxidative stress should be important component of cardiomyocyte proliferation-based therapeutic approaches.

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Metadata

Authors
Puente, B. N., Kimura, W., Muralidhar, S. A., Moon, J., Amatruda, J. F., Phelps, K. L., Grinsfelder, D., Rothermel, B. A., Chen, R., Garcia, J. A., Santos, C. X., Thet, S., Mori, E., Kinter, M. T., Rindler, P. M., Zacchigna, S., Mukherjee, S., Chen, D. J., Mahmoud, A. I., Giacca, M., Rabinovitch, P. S., Asaithamby, A., Shah, A. M., Szweda, L. I., & Sadek, H. A.
Venue
Cell
Publisher
Elsevier BV
Published
2014-04
Volume
157
Issue
3
Pages
565-579
ISSN
0092-8674 (ISSN-L)
DOI
10.1016/j.cell.2014.03.032
OpenAlex
W2035847235
Cited by
909
References
13
FWCI
18.50
Type
journal article
Language
en
Open access
bronze

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Puente, B. N., Kimura, W., Muralidhar, S. A., Moon, J., Amatruda, J. F., Phelps, K. L., Grinsfelder, D., Rothermel, B. A., Chen, R., Garcia, J. A., Santos, C. X., Thet, S., Mori, E., Kinter, M. T., Rindler, P. M., Zacchigna, S., Mukherjee, S., Chen, D. J., Mahmoud, A. I., . . . Sadek, H. A. (2014). The Oxygen-Rich Postnatal Environment Induces Cardiomyocyte Cell-Cycle Arrest through DNA Damage Response. Cell. https://doi.org/10.1016/j.cell.2014.03.032

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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.