2016
DOI: 10.18632/aging.101098
View full text |Buy / Rent full text
|
Sign up to set email alerts
|

Abstract: Skeletal muscle is a highly regenerative tissue, but muscle repair potential is increasingly compromised with advancing age. In this study, we demonstrate that increased NF-κB activity in aged muscle fibers contributes to diminished myogenic potential of their associated satellite cells. We further examine the impact of genetic modulation of NF-κB signaling in muscle satellite cells or myofibers on recovery after damage. These studies reveal that NF-κB activity in differentiated myofibers is sufficient to driv… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1
1

Citation Types

0
50
1

Year Published

2017
2017
2018
2018

Publication Types

Select...
4

Relationship

2
2

Authors

Journals

citations
Cited by 50 publications
(51 citation statements)
references
References 52 publications
(51 reference statements)
0
50
1
Order By: Relevance
“…reported that muscle from MISR mice did not become atrophic when subjected to denervation and cancer (Cai et al ., ). Protection from denervation, unloading, immobilization, endotoxin administration, and cryoinjury also have been reported using different models of suppressed NFκB signaling (Hunter & Kandarian, ; Mourkioti et al ., ; Judge et al ., ; Van Gammeren et al ., ; Haegens et al ., ; Okazaki et al ., ; Oh et al ., ). The resistance conferred by NFκB axis suppression to these atrophy‐inducing stimuli indicates that NFκB has opposing effects (both negative and positive) on muscle development and health, depending on the level of flux ( i.e ., dosage) through the pathway.…”
Section: Discussionmentioning
confidence: 97%
“…Lastly, NFκB is thought to control satellite cell function and their dysfunction during development could have resulted in reduced muscle mass. Yet, this possibility seems less likely because myogenic colony formation efficiency and satellite cell frequency are not affected in young MISR mice (Oh et al ., ).…”
Section: Discussionmentioning
confidence: 97%
“…Preventing chronic activation of the pro-inflammatory NFkB/Rel and JAK/STAT signaling pathways in the fly intestine promotes regenerative homeostasis and extends lifespan (Guo et al, 2014; Li et al, 2016b). In the mammalian skeletal muscle, an age specific increase in niche-derived NF‐κB signaling impairs satellite cells function, which can be attenuated by systemic administration of sodium salicylate, an FDA‐approved NF‐κB inhibitor (Oh et al, 2016). Observations in humans, in turn, suggest a central role for NF-κB activation and TNFα signaling in skin aging (Haustead et al, 2016).…”
Section: Aging Roadblocks and Targets For Improvementmentioning
confidence: 99%
“…The SASP is an example of a cell non-autonomous means of spreading aging-states throughout a tissue. Other examples of cell non-autonomous aging include age-related NFkB signaling in muscle fibers controlling the activity of satellite cells[50], intestinal cells signalling to neurons to propagate the health and longevity benefits of diet restriction[51,52], and epithelial cells in breast communicating age-states through a cell-cell contact-dependent mechanism[29]. The multiple ratcheting mechanisms of aging that are at work in tissues suggest aging may be irreversible.…”
Section: Metastability Of Aging Phenotypesmentioning
confidence: 99%
“…This procedure generates a reproducible injury in the muscle with a discrete border between uninjured and injured muscle (28, 29). Injured muscles were allowed to recover for 5 days prior to mouse euthanasia and muscle harvest.…”
Section: Animals and Methodsmentioning
confidence: 99%