2015
DOI: 10.18632/aging.100802
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Abstract: Functional competence and self-renewal of mammalian skeletal muscle myofibers and progenitor cells declines with age. Progression of the muscle aging phenotype involves the decline of juvenile protective factors i.e., proteins whose beneficial functions translate directly to the quality of life, and self-renewal of progenitor cells. These characteristics occur simultaneously with the age-associated increase of p38α stress response signaling. This suggests that the maintenance of low levels of p38α activity of … Show more

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Cited by 24 publications
(28 citation statements)
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References 62 publications
(101 reference statements)
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“…Consistent with the notion that p38α is a significant regulator of cell senescence, aged DN-p38α AF/+ mice are resistant to age-dependent decline in the proliferation and regeneration of several peripheral tissue progenitors when compared to wild-type littermates (Papaconstantinou et al, 2009, 2015; Wong et al, 2009). This has led to the hypothesis that in the periphery, p38 modulates the regenerative capacity of tissues that rely upon a progenitor population (e.g., muscle, liver, and pancreas).…”
Section: 0 Introductionsupporting
confidence: 67%
“…Consistent with the notion that p38α is a significant regulator of cell senescence, aged DN-p38α AF/+ mice are resistant to age-dependent decline in the proliferation and regeneration of several peripheral tissue progenitors when compared to wild-type littermates (Papaconstantinou et al, 2009, 2015; Wong et al, 2009). This has led to the hypothesis that in the periphery, p38 modulates the regenerative capacity of tissues that rely upon a progenitor population (e.g., muscle, liver, and pancreas).…”
Section: 0 Introductionsupporting
confidence: 67%
“…Paradoxically, in addition to its known role in satellite cell activation 76 , p38 α/β-MAPK signalling can also activate p16 Ink4a to promote cellular senescence 99 . A genetic link between p38α/β-MAPK and p16 Ink4a was recently demonstrated in skeletal muscle, when it was found that p16 Ink4a protein levels were reduced in the gastrocnemius muscle of animals expressing a dominant-negative p38α allele, although future studies will need to verify this connection in satellite cells 100 . Cumulatively, these data suggest that an age-regulated intrinsic p38 signalling-axis exists in the satellite cell pool.…”
Section: Satellite Cell Fate In Aging Musclementioning
confidence: 94%
“…Demonstration that the decreased expresion of p38α/β and its targeted activation of aging phenotype markers addresses this question in that; a) inhibition of p38α/β decreases the expression of markers of aging; b) the attenuation of p38α/β in a haploinsuficient p38α +/− mouse delays the aging of pancreatic β-cells and skeletal muscle progenitor cells [134,136]. The p38MAPK inhibitors provide an experimental linkage of the molecular mechanisms activated by inflammtion-oxidative stress to the molecular mechanisms of initiation of PTB and pPROM.…”
Section: Significancementioning
confidence: 99%