2014
DOI: 10.18632/aging.100696 View full text |Buy / Rent full text
|
|

Abstract: Accumulation of reactive oxygen species (ROS) in skeletal muscles and the resulting decline in muscle performance are hallmarks of sarcopenia. However, the precise mechanism by which ROS results in a decline in muscle performance is unclear. We demonstrate that isometric-exercise concomitantly increases the activities of Silent information regulator 1 (SIRT-1) and Poly [ADP-ribose] polymerase (PARP-1), and that activated SIRT-1 physically binds with and inhibits PARP-1 activity by a deacetylation dependent mec… Show more

Help me understand this report

Search citation statements

Order By: Relevance
Select...
2
1
1
1
1
57
0

Year Published

2015
2015
2017
2017

Publication Types

Select...
4

Relationship

1
3

Authors

Journals

1
57
0
Order By: Relevance
“…In particular, at the same time that PARPs appear to have a beneficial effect on the control of DNA integrity and may positively contribute to an increase in organismal longevity, its over-activation during the aging process may contribute to cellular NAD decline and metabolic dysfunction (Figure 4). Interestingly, this appears to be the case, since it was proposed that over-activation of PARP1 in skeletal muscle of old mice during exercise can lead to cellular NAD decline that may contribute to exercise-induced fatigue and reduced muscle performance in response to exercise during aging (Mohamed et al, 2014). …”
Section: What Causes the Nad Decline Observed During The Aging Process?mentioning
Create an account to read the remaining citation statements from this report. You will also get access to:
  • Search over 1.2b+ citation statments to see what is being said about any topic in the research literature
  • Advanced Search to find publications that support or contrast your research
  • Citation reports and visualizations to easily see what publications are saying about each other
  • Browser extension to see Smart Citations wherever you read research
  • Dashboards to evaluate and keep track of groups of publications
  • Alerts to stay on top of citations as they happen
  • Automated reference checks to make sure you are citing reliable research in your manuscripts
  • 7 day free preview of our premium features.

Trusted by researchers and organizations around the world

Over 130,000 students researchers, and industry experts at use scite

See what students are saying

rupbmjkragerfmgwileyiopcupepmcmbcthiemesagefrontiersapsiucrarxivemeralduhksmucshluniversity-of-gavle
“…In particular, at the same time that PARPs appear to have a beneficial effect on the control of DNA integrity and may positively contribute to an increase in organismal longevity, its over-activation during the aging process may contribute to cellular NAD decline and metabolic dysfunction (Figure 4). Interestingly, this appears to be the case, since it was proposed that over-activation of PARP1 in skeletal muscle of old mice during exercise can lead to cellular NAD decline that may contribute to exercise-induced fatigue and reduced muscle performance in response to exercise during aging (Mohamed et al, 2014). …”
Section: What Causes the Nad Decline Observed During The Aging Process?mentioning
“…This includes identifying the mitochondrial modifications that are reversible by exercise and nutritional interventions in aging. For example, mitochondrial acetylation is reversible at least under some circumstances including exercise (97). Proteins like SIRT1 and SIRT3 may be important regulators of deacetylation in mitochondria (46, 97, 132).…”
Section: Foxo Proteins and The Ubiquitin Proteasome System (Ups) In Mmentioning
“…For example, mitochondrial acetylation is reversible at least under some circumstances including exercise (97). Proteins like SIRT1 and SIRT3 may be important regulators of deacetylation in mitochondria (46, 97, 132). SIRT1 is important for deacetylation of mitochondrial-interacting targets like PGC-1α, FOXO3, p53 and NF-kB (Reviewed in (13, 110) and has been implicated in improving function and life span in aging (95).…”
Section: Foxo Proteins and The Ubiquitin Proteasome System (Ups) In Mmentioning
“…Reduced skeletal muscle performance in response to exercise in aged mice is associated with lower activity of SIRT1 in this tissue, which is in turn related to an increase in poly (ADP-ribose) polymerase (PARP-1) activity that diminishes intracellular NAD levels. Increment of SIRT1 activity by PARP-1 inhibition results in higher skeletal muscle mitochondrial biogenesis and performance (Mohamed et al, 2014). Moreover, SIRT1 activity up-regulation is likely involved in the protective effects of exercise training on aged skeletal muscle in rats (Koltai et al, 2010).…”
Section: Sirtuinsmentioning