ArticleFrontiers in cellular neuroscience2013
When is Sirt1 activity bad for dying neurons?
Article in Frontiers in cellular neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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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.
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Who cites it
13 citing papers in PubMed, 24 citations in OpenAlex.
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- Changes in Stress-Mediated Markers in a Human Cardiomyocyte Cell Line under Hyperglycemia.International journal of molecular sciences · 2021Article
- Towards resolving the enigma of the dichotomy of resveratrol: cis- and trans-resveratrol have opposite effects on TyrRS-regulated PARP1 activation.GeroScience · 2021Article
- Sensory Neuromodulation.Frontiers in systems neuroscience · 2020Article
- Sirtuins in Neuroendocrine Regulation and Neurological Diseases.Frontiers in neuroscience · 2018Review
- Sirtuins and Their Roles in Brain Aging and Neurodegenerative Disorders.Neurochemical research · 2017Review
- Is SIRT6 Activity Neuroprotective and How Does It Differ from SIRT1 in This Regard?Frontiers in cellular neuroscience · 2017Article
- Hepatic SirT1-Dependent Gain of Function of Stearoyl-CoA Desaturase-1 Conveys Dysmetabolic and Tumor Progression Functions.Cell reports · 2015Article
- SIRT1 in the brain-connections with aging-associated disorders and lifespan.Frontiers in cellular neuroscience · 2015Review
- WISP1: Clinical insights for a proliferative and restorative member of the CCN family.Current neurovascular research · 2014Review
- BRCA1 as a nicotinamide adenine dinucleotide (NAD)-dependent metabolic switch in ovarian cancer.Cell cycle (Georgetown, Tex.) · 2014Article
- Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sirt1, the class III histone deacetylase, is generally associated with increased life span and with a pro-survival effect in neurons stressed by pathological factors. Recent work, however, suggests that Sirt1 silencing could also promote neuronal survival. A possible reason suggested is Sirt1 silencing enhanced expression of both IGF-1 and IGF-1 receptor, signaling from which promotes survival. This work adds to the small but steady stream of findings that are diametrically opposite to the overwhelmingly large amount of evidence supporting a beneficial effect of sustaining or enhancing Sirt1 activity in neuronal injuries and diseases. We attempt to reconcile this discrepancy below by noting evidence that elevated Sirt1 levels and/or activity may not help, and could even adversely exacerbates demise, during events of acute neuronal damage or death. However, sustained Sirt1 activation will be beneficial in situations of chronic and long-term sub-lethal stresses, and the status of IGF-1 signaling may influence Sirt1 action in a context dependent manner.
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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.