Atypically Shaped Cardiomyocytes (ACMs): The Identification, Characterization and New Insights into a Subpopulation of Cardiomyocytes
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- Mariko Omatsu-Kanbe
- Department of Physiology, Shiga University of Medical Science, Otsu 520-2192, Shiga, Japan
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- Ryo Fukunaga
- Department of Physiology, Shiga University of Medical Science, Otsu 520-2192, Shiga, Japan
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- Xinya Mi
- Department of Physiology, Shiga University of Medical Science, Otsu 520-2192, Shiga, Japan
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- Hiroshi Matsuura
- Department of Physiology, Shiga University of Medical Science, Otsu 520-2192, Shiga, Japan
書誌事項
- 公開日
- 2022-06-27
- 資源種別
- journal article
- 権利情報
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- https://creativecommons.org/licenses/by/4.0/
- DOI
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- 10.3390/biom12070896
- 公開者
- MDPI AG
説明
<jats:p>In the adult mammalian heart, no data have yet shown the existence of cardiomyocyte-differentiable stem cells that can be used to practically repair the injured myocardium. Atypically shaped cardiomyocytes (ACMs) are found in cultures of the cardiomyocyte-removed fraction obtained from cardiac ventricles from neonatal to aged mice. ACMs are thought to be a subpopulation of cardiomyocytes or immature cardiomyocytes, most closely resembling cardiomyocytes due to their spontaneous beating, well-organized sarcomere and the expression of cardiac-specific proteins, including some fetal cardiac gene proteins. In this review, we focus on the characteristics of ACMs compared with ventricular myocytes and discuss whether these cells can be substitutes for damaged cardiomyocytes. ACMs reside in the interstitial spaces among ventricular myocytes and survive under severely hypoxic conditions fatal to ventricular myocytes. ACMs have not been observed to divide or proliferate, similar to cardiomyocytes, but they maintain their ability to fuse with each other. Thus, it is worthwhile to understand the role of ACMs and especially how these cells perform cell fusion or function independently in vivo. It may aid in the development of new approaches to cell therapy to protect the injured heart or the clarification of the pathogenesis underlying arrhythmia in the injured heart.</jats:p>
収録刊行物
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- Biomolecules
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Biomolecules 12 (7), 896-, 2022-06-27
MDPI AG