2016
DOI: 10.1152/ajpcell.00176.2016
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The myonuclear domain is not maintained in skeletal muscle during either atrophy or programmed cell death

Abstract: Skeletal muscle mass can increase during hypertrophy or decline dramatically in response to normal or pathological signals that trigger atrophy. Many reports have documented that the number of nuclei within these cells is also plastic. It has been proposed that a yet-to-be-defined regulatory mechanism functions to maintain a relatively stable relationship between the cytoplasmic volume and nuclear number within the cell, a phenomenon known as the "myonuclear domain" hypothesis. While it is accepted that hypert… Show more

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Cited by 20 publications
(31 citation statements)
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“…However, linkage of myonuclei number and muscle fiber size is the basis of the “myonuclear domain” hypothesis which asserts that a single myonucleus controls the translational and transcriptional regulation of protein synthesis for a limited cell volume known as the myonuclear domain. Although more recent studies indicate that age‐related myofiber atrophy results primarily from reductions in myonuclear domain size instead of the loss of myonuclei numbers (Karlsen et al, 2015; Schwartz, Brown, McLaughlin, Smith, & Bigelow, 2016), other findings show that increased myonuclear fusion facilitates muscle hypertrophy, especially when the myonuclear domain size exceeds a certain threshold (Jo et al, 2012; Petrella, Kim, Cross, Kosek, & Bamman, 2006). The findings in the current study support the possibility that the ablation of TNF‐α contributes to increased myofiber size in aging muscle by increasing the frequency of muscle cell fusion with aging muscle fibers.…”
Section: Discussionmentioning
confidence: 99%
“…However, linkage of myonuclei number and muscle fiber size is the basis of the “myonuclear domain” hypothesis which asserts that a single myonucleus controls the translational and transcriptional regulation of protein synthesis for a limited cell volume known as the myonuclear domain. Although more recent studies indicate that age‐related myofiber atrophy results primarily from reductions in myonuclear domain size instead of the loss of myonuclei numbers (Karlsen et al, 2015; Schwartz, Brown, McLaughlin, Smith, & Bigelow, 2016), other findings show that increased myonuclear fusion facilitates muscle hypertrophy, especially when the myonuclear domain size exceeds a certain threshold (Jo et al, 2012; Petrella, Kim, Cross, Kosek, & Bamman, 2006). The findings in the current study support the possibility that the ablation of TNF‐α contributes to increased myofiber size in aging muscle by increasing the frequency of muscle cell fusion with aging muscle fibers.…”
Section: Discussionmentioning
confidence: 99%
“…The plastic nature of muscle, and its syncytial status, has given rise to a controversy in the field that only recently appears to have been resolved-the "myonuclear domain hypothesis" [7][8][9]. This theory has its origins in the concept of "Wirkungssphäre, " or "sphere of influence," proposed by Strassburger in 1893 [10], in which he argued that a nucleus can only support a descrete volume of cytoplasm, which in turn defines the upper limits to cell size.…”
Section: Commentarymentioning
confidence: 99%
“…We used two independent methods to monitor nuclear fate during both atrophy and death in this model [7]. The first was a standard anatomical approach.…”
Section: Commentarymentioning
confidence: 99%
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