» Articles » PMID: 35883452

Atypically Shaped Cardiomyocytes (ACMs): The Identification, Characterization and New Insights into a Subpopulation of Cardiomyocytes

Overview
Journal Biomolecules
Publisher MDPI
Date 2022 Jul 27
PMID 35883452
Authors
Affiliations
Soon will be listed here.
Abstract

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.

Citing Articles

Mesenchymal stem cells derived exosomes: a new era in cardiac regeneration.

Rayat Pisheh H, Sani M Stem Cell Res Ther. 2025; 16(1):16.

PMID: 39849585 PMC: 11756228. DOI: 10.1186/s13287-024-04123-2.


Roles of prion proteins in mammalian development.

Cheon Y, Ryou C, Svedruzic Z Anim Cells Syst (Seoul). 2024; 28(1):551-566.

PMID: 39664939 PMC: 11633422. DOI: 10.1080/19768354.2024.2436860.


Immunolocalization of Matrix Metalloproteinases 2 and 9 and Their Inhibitors in the Hearts of Rats Treated with Immunosuppressive Drugs-An Artificial Intelligence-Based Digital Analysis.

Wilk A, Krol M, Kielbowski K, Bakinowska E, Szumilas K, Surowka A Biomedicines. 2024; 12(4).

PMID: 38672125 PMC: 11048150. DOI: 10.3390/biomedicines12040769.


Molecular Pathogenesis of Cardiac Arrhythmia.

Okamoto Y, Ono K Biomolecules. 2022; 12(10).

PMID: 36291601 PMC: 9599332. DOI: 10.3390/biom12101393.

References
1.
Tallquist M, Molkentin J . Redefining the identity of cardiac fibroblasts. Nat Rev Cardiol. 2017; 14(8):484-491. PMC: 6329009. DOI: 10.1038/nrcardio.2017.57. View

2.
Dick S, Macklin J, Nejat S, Momen A, Clemente-Casares X, Althagafi M . Self-renewing resident cardiac macrophages limit adverse remodeling following myocardial infarction. Nat Immunol. 2018; 20(1):29-39. PMC: 6565365. DOI: 10.1038/s41590-018-0272-2. View

3.
Kurose H . Cardiac Fibrosis and Fibroblasts. Cells. 2021; 10(7). PMC: 8306806. DOI: 10.3390/cells10071716. View

4.
Honjo H, Boyett M, Kodama I, TOYAMA J . Correlation between electrical activity and the size of rabbit sino-atrial node cells. J Physiol. 1996; 496 ( Pt 3):795-808. PMC: 1160865. DOI: 10.1113/jphysiol.1996.sp021728. View

5.
van Berlo J, Kanisicak O, Maillet M, Vagnozzi R, Karch J, Lin S . c-kit+ cells minimally contribute cardiomyocytes to the heart. Nature. 2014; 509(7500):337-41. PMC: 4127035. DOI: 10.1038/nature13309. View