ArticleAging2014
Dysregulation of SIRT-1 in aging mice increases skeletal muscle fatigue by a PARP-1-dependent mechanism.
Article in Aging, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
48 citing papers in PubMed, 1 synthesis or guideline pooled it, 81 citations in OpenAlex.
- Myokine Signaling in Sarcopenia-Associated Chronic Musculoskeletal Pain: A Systematic Review of Inflammatory Mechanisms.International journal of molecular sciences · 2026Pooled it
- Divergent serum metabolomic, skeletal muscle signaling, transcriptomic, and performance adaptations to fasted versus whey protein-fed sprint interval training.American journal of physiology. Endocrinology and metabolism · 2021Trial
- Effects of aging and resistance exercise on muscle strength, physiological properties, longevity proteins, and telomere length in SAMP8 mice.Biogerontology · 2025Article
- Protein Acetylation and NAD+ Homeostasis in Aging Muscle.Advances in experimental medicine and biology · 2025Review
- Resveratrol Inhibits Nucleosome Binding and Catalytic Activity of PARP1.Biomolecules · 2024Article
- TRIM16 facilitates SIRT-1-dependent regulation of antioxidant response to alleviate age-related sarcopenia.Journal of cachexia, sarcopenia and muscle · 2024Article
- Bone-organ axes: bidirectional crosstalk.Military Medical Research · 2024Review
- Tankyrase-1 regulates RBP-mediated mRNA turnover to promote muscle fiber formation.Nucleic acids research · 2024Article
- Impact of Exercise Training on Survival Rate and Neural Cell Death in Sepsis Through the Maintenance of Redox Equilibrium.International neurourology journal · 2024Article
- The Impact of 8 Weeks of Combined Physical Exercise Training on SIRT3 and mTOR in Lymphocytes, and on Lipid Peroxidation.Healthcare (Basel, Switzerland) · 2024Article
- PARP1 mediated PARylation contributes to myogenic progression and glucocorticoid transcriptional response.Cell death discovery · 2023Article
- The Role of Sirtuins in Sarcopenia and Frailty.Aging and disease · 2023Article
- Mitochondria transplant therapy improves regeneration and restoration of injured skeletal muscle.Journal of cachexia, sarcopenia and muscle · 2023Article
- Epithelial NADFrontiers in immunology · 2023Article
- CYB5R3 overexpression preserves skeletal muscle mitochondria and autophagic signaling in aged transgenic mice.GeroScience · 2022Article
- Post-translational Modifications: The Signals at the Intersection of Exercise, Glucose Uptake, and Insulin Sensitivity.Endocrine reviews · 2022Review
- Article
- NADMolecular and cellular biochemistry · 2022Review
- Review
- Skeletal Muscle Gene Expression Profile in Response to Caloric Restriction and Aging: A Role for SirT1.Genes · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
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 mechanism in skeletal muscle from young mice. In contrast, skeletal muscle from aged mice displays higher PARP-1 activity and lower SIRT-1 activity due to decreased intracellular NAD+ content, and as a result reduced muscle performance in response to exercise. Interestingly, injection of PJ34, a PARP-1 inhibitor, in aged mice increased SIRT-1 activity by preserving intracellular NAD+ content, which resulted in higher skeletal muscle mitochondrial biogenesis and performance. We found that the higher activity of PARP-1 in H2O2-treated myotubes or in exercised-skeletal muscles from aged mice is due to an elevated level of PARP-1 acetylation by the histone acetyltransferase General control of amino acid synthesis protein 5-like 2 (GCN-5). These results suggest that activation of SIRT-1 and/or inhibition of PARP-1 may ameliorate skeletal muscle performance in pathophysiological conditions such as sarcopenia and disuse-induced atrophy in aging.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.