2016
DOI: 10.18632/aging.101039
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Abstract: Skeletal muscle mass and power decrease with age, leading to impairment of mobility and metabolism in the elderly. Ca2+ signaling is crucial for myoblast differentiation as well as muscle contraction through activation of transcription factors and Ca2+-dependent kinases and phosphatases. Ca2+ channels, such as dihydropyridine receptor (DHPR), two-pore channel (TPC) and inositol 1,4,5-triphosphate receptor (ITPR), function to maintain Ca2+ homeostasis in myoblasts. Here, we observed a significant decrease in ex… Show more

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Cited by 14 publications
(8 citation statements)
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References 50 publications
(60 reference statements)
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“…To our knowledge, this is the first study to demonstrate that systemic treatment of aged animals with a small molecule drug-like NNMT inhibitor [38,39] can rejuvenate muSCs, thereby robustly promoting muSC activation and fusion which are critical to support de novo myofiber regeneration and repair following injury [14][15][16]. At 1-week post-injury, control aged mice showed poor myofiber growth, minimal muSC activity, and a compromised skeletal muscle repair profile; these observations were consistent with impaired muSC regenerative capacity previously reported in skeletal muscles from aged mice [45,46]. In contrast, aged mice treated with NNMTi demonstrated dramatically increased frequency of activated muSCs and greatly enhanced muscle repair via muSC fusion and subsequent myonuclear accrual.…”
Section: Discussionsupporting
confidence: 88%
See 1 more Smart Citation
“…To our knowledge, this is the first study to demonstrate that systemic treatment of aged animals with a small molecule drug-like NNMT inhibitor [38,39] can rejuvenate muSCs, thereby robustly promoting muSC activation and fusion which are critical to support de novo myofiber regeneration and repair following injury [14][15][16]. At 1-week post-injury, control aged mice showed poor myofiber growth, minimal muSC activity, and a compromised skeletal muscle repair profile; these observations were consistent with impaired muSC regenerative capacity previously reported in skeletal muscles from aged mice [45,46]. In contrast, aged mice treated with NNMTi demonstrated dramatically increased frequency of activated muSCs and greatly enhanced muscle repair via muSC fusion and subsequent myonuclear accrual.…”
Section: Discussionsupporting
confidence: 88%
“…In contrast, aged mice treated with NNMTi demonstrated dramatically increased frequency of activated muSCs and greatly enhanced muscle repair via muSC fusion and subsequent myonuclear accrual. Both the number of activated muSC and the average size of regenerating myofibers on the injured limb had nearly doubled at 1-week post-injury with treatment facilitating the development of myofibers with much larger cross-sectional areas, similar to youthful myogenic growth response [45,46]. Consistent with increased muscle fiber growth, NNMTi treatment nearly doubled peak dorsiflexor torque output on the injured limb, suggesting clinically meaningful overall improvements in muscle strength and function.…”
Section: Discussionmentioning
confidence: 83%
“…The vital mechanism underlying proliferation and differentiation in mSCs is highly conserved in both primary and C2C12 myoblast cultures in vitro [50]. Myoblast differentiation is indispensable for muscle regeneration; however, the initial burst of myoblast proliferation is also essential for this process [51,52]. In this study, we observed that both USCs-EVs and iMSCs-EVs promoted C2C12 myoblast proliferation.…”
Section: Discussionmentioning
confidence: 51%
“…A follow-up study found that the IP3 genes were expressed in embryos and placenta very early during placentation [33], and the growth retardation may result from impairment of vascularization of the placenta and other extra-embryonic tissues [33]. Decreased expression of itpr1 has also been found in aged mice skeletal muscle [34]. Therefore, we hypothesized that…”
Section: Relationship Between Itpr1 Gene Expression and Placental Epimentioning
confidence: 98%