ArticleAging2009
Poly(ADP-ribose) polymerase 1 at the crossroad of metabolic stress and inflammation in aging.
Article in Aging, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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.
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
40 citing papers in PubMed, 75 citations in OpenAlex.
- Article
- NADCell communication and signaling : CCS · 2024Review
- The Central Role of the NAD+ Molecule in the Development of Aging and the Prevention of Chronic Age-Related Diseases: Strategies for NAD+ Modulation.International journal of molecular sciences · 2023Review
- NADCells · 2022Review
- Evolution of a histone variant involved in compartmental regulation of NAD metabolism.Nature structural & molecular biology · 2021Article
- Review
- The taming of PARP1 and its impact on NADMolecular metabolism · 2020Review
- MacroH2A1 Regulation of Poly(ADP-Ribose) Synthesis and Stability Prevents Necrosis and Promotes DNA Repair.Molecular and cellular biology · 2019Article
- Novel insights into PARPs in gene expression: regulation of RNA metabolism.Cellular and molecular life sciences : CMLS · 2019Review
- NADPNature communications · 2019Article
- Role of Nicotinamide Adenine Dinucleotide and Related Precursors as Therapeutic Targets for Age-Related Degenerative Diseases: Rationale, Biochemistry, Pharmacokinetics, and Outcomes.Antioxidants & redox signaling · 2019Review
- Hepatic DNA Damage Induced by Electronic Cigarette Exposure Is Associated With the Modulation of NAD+/PARP1/SIRT1 Axis.Frontiers in endocrinology · 2019Article
- Cancer Etiology: A Metabolic Disease Originating from Life's Major Evolutionary Transition?Oxidative medicine and cellular longevity · 2019Review
- ERCC1-deficient cells and mice are hypersensitive to lipid peroxidation.Free radical biology & medicine · 2018Article
- Analysis of PARP inhibitor toxicity by multidimensional fluorescence microscopy reveals mechanisms of sensitivity and resistance.Nature communications · 2018Article
- Article
- MacroH2A1.1 regulates mitochondrial respiration by limiting nuclear NADNature structural & molecular biology · 2017Article
- Flow signaling and atherosclerosis.Cellular and molecular life sciences : CMLS · 2017Review
- New Quantitative Mass Spectrometry Approaches Reveal Different ADP-ribosylation Phases Dependent On the Levels of Oxidative Stress.Molecular & cellular proteomics : MCP · 2017Article
- 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
Poly(ADP-ribose) polymerase 1 (PARP1) is a chromatin-associated nuclear protein, which functions as molecular stress sensor. Reactive oxygen species, responsible for the most plausible and currently acceptable global mechanism to explain the aging process, strongly activate the enzymatic activity of PARP1 and the formation of poly(ADP-ribose) (PAR) from NAD(+). Consumption of NAD(+) links PARP1 to energy metabolism and to a large number of NAD(+)-dependent enzymes, such as the sirtuins. As transcriptional cofactor for NF-kappaB-dependent gene expression, PARP1 is also connected to the immune response, which is implicated in almost all age-related or associated diseases. Accordingly, numerous experimental studies have demonstrated the beneficial effects of PARP inhibition for several age-related diseases. This review summarizes recent findings on PARP1 and puts them in the context of metabolic stress and inflammation 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.