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

Biomolecules. 2022 Jun 27;12(7):896. doi: 10.3390/biom12070896.

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.

Keywords: ACMs; atypically shaped cardiomyocytes; cardiac ventricle; cardiomyocyte; cell fusion; fetal cardiac gene proteins; heart; ischemic resistance; spontaneous beating; subpopulation of cardiomyocytes.

Publication types

  • Review
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cells, Cultured
  • Heart Ventricles / pathology
  • Mammals
  • Mice
  • Myocardium* / metabolism
  • Myocytes, Cardiac* / metabolism
  • Proteins / metabolism
  • Stem Cells

Substances

  • Proteins

Grant support

This work was supported by a Grant-in-Aid for Scientific Research (C) from the Japan Society for the Promotion of Science (18K06871 and 21K06768 to M.O.-K.).