Sentence examples for muscle cell aging from inspiring English sources

We suggest that PABPN1 regulates muscle cell aging.

Together, these studies indicate that reduced levels of PABPN1 induce muscle cell aging.

We suggest that PABPN1 levels regulate muscle cell aging and OPMD represents an accelerated muscle aging disorder.

In culture, PABPN1 down-regulation induces muscle cell aging and myogenesis defects that are proportional to a decrease in PABPN1 levels.

Here we show that in addition to myogenesis defects, PABPN1 down-regulation induces phenotypes of muscle cell aging, including reduced cell growth rate, heterochromatic foci formation, reduced mitochondrial metabolic rate, fat droplets formation and increased sensitivity to oxidative stress.

We report here that in colonic smooth muscle cells aging impairs IP3R-and RyR-mediated Ca2+ release, suggesting that age influences this signaling system in a tissue-specific way.

In rat vascular smooth muscle cells, AGEs treatment inhibits the phosphorylation of Akt and mTOR [ 23].

Revealed cellular and molecular mechanisms of human muscle stem cell aging, prompted us to examine whether forced Notch activation would be able to restore myogenic responses to old human satellite cells cultured with aged human sera (old isochronic cultures).

These data are the first to demonstrate that cellular and molecular mechanisms of muscle stem cell aging are highly conserved between mouse and human, with respect to the age-specific decline in satellite cell activation and to the biochemical imbalance in TGF-β and Notch.

However, the canonical model of muscle stem cell aging postulates that a decline in such mitogens over time leads to reduced activation of satellite cells that are resident to old tissue [ 1, 24, 25], so we explored these phenomena in more detail.

Furthermore, the sustained activation of Wnt signaling in skeletal muscle is associated with stem cell aging and the transformation of myogenic to fibrotic tissue [ 46].