Myocytes, Mitochondria, and Maturation

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Science  14 Oct 2011:
Vol. 334, Issue 6053, pp. 158
DOI: 10.1126/science.334.6053.158-d

Understanding the factors and events required for normal heart development will hopefully provide insight into how to treat heart disease and other cardiac abnormalities. Mitochondrial function is essential in cardiac cells, with mitochondria transitioning from an immature to mature state in the embryo. How this occurs, however, is not well understood. During early embryonic development, Hom et al. find that mitochondria alter their length, network complexity, and area, becoming more mature. This corresponds with a decrease in reactive oxygen species in cardiomyocytes and their differentiation. Genetic and pharmacological inhibition showed that these changes are probably the result of the closure of mitochondrial permeability transition pores (mPTPs). mPTP closure increased ATP production needed for myocyte function and drove myocyte differentiation through redox signaling. Thus, the maturation of mitochondria signals cardiomyocyte differentiation.

Dev. Cell 21, 469 (2011).

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