Evidence map›Paper›PMID 27240523›Full record

ArticleScientific reports2016

Exogenous NAD(+) decreases oxidative stress and protects H2O2-treated RPE cells against necrotic death through the up-regulation of autophagy.

Ying Zhu, Ke-Ke Zhao, Yao Tong, Ya-Li Zhou, Yi-Xiao Wang, Pei-Quan Zhao, Zhao-Yang Wang

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
4.5field-weighted citation impact, top 5% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

41 citing papers in PubMed, 65 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. NADMolecular biology reports · 2023
    Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Mitophagy: An Emerging Target in Ocular Pathology.Investigative ophthalmology & visual science · 2021
    Review
  16. Exogenous NADAntioxidants (Basel, Switzerland) · 2021
    Article
  17. Spermidine Attenuates Oxidative Stress-Induced Apoptosis via Blocking CaInternational journal of molecular sciences · 2021
    Article
  18. Article
  19. Article
  20. Codonopsis pilosula Polysaccharides Alleviate AβCurrent Alzheimer research · 2021
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Ying ZhuDepartment of Ophthalmology, Xinhua Hospital, Shanghai Jiaotong University Scool of Medicine, Shanghai, China.
Ke-Ke ZhaoDepartment of Ophthalmology, Shanghai Children's Medical Center, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Yao TongDepartment of Ophthalmology, Xinhua Hospital, Shanghai Jiaotong University Scool of Medicine, Shanghai, China.
Ya-Li ZhouDepartment of Ophthalmology, Xinhua Hospital, Shanghai Jiaotong University Scool of Medicine, Shanghai, China.
Yi-Xiao WangDepartment of Ophthalmology, Xinhua Hospital, Shanghai Jiaotong University Scool of Medicine, Shanghai, China.
Pei-Quan ZhaoDepartment of Ophthalmology, Xinhua Hospital, Shanghai Jiaotong University Scool of Medicine, Shanghai, China.
Zhao-Yang WangDepartment of Ophthalmology, Xinhua Hospital, Shanghai Jiaotong University Scool of Medicine, Shanghai, China.
XinHua Hospital · CNShanghai Children's Medical Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Increased oxidative stress, which can lead to the retinal pigment epithelium (RPE) cell death by inducing ATP depletion and DNA repair, is believed to be a prominent pathology in age-related macular degeneration (AMD). In the present study, we showed that and 0.1 mM nicotinamide adenine dinucleotide (NAD(+)) administration significantly blocked RPE cell death induced by 300 μM H2O2. Further investigation showed that H2O2 resulted in increased intracellular ROS level, activation of PARP-1 and subsequently necrotic death of RPE cells. Exogenous NAD(+) administration significantly decreased intracellular and intranuclear ROS levels in H2O2-treated RPE cells. In addition, NAD(+) administration to H2O2-treated RPE cells inhibited the activation of PARP-1 and protected the RPE cells against necrotic death. Moreover, exogenous NAD(+) administration up-regulated autophagy in the H2O2-treated RPE cells. Inhibition of autophagy by LY294002 blocked the decrease of intracellular and intranuclear ROS level. Besides, inhibition of autophagy by LY294002 abolished the protection of exogenous NAD(+) against H2O2-induced cell necrotic death. Taken together, our findings indicate that that exogenous NAD(+) administration suppresses H2O2-induced oxidative stress and protects RPE cells against PARP-1 mediated necrotic death through the up-regulation of autophagy. The results suggest that exogenous NAD(+) administration might be potential value for the treatment of AMD.

Indexed as

AutophagyCells, CulturedCell SurvivalChromonesHumansHydrogen PeroxideMacular DegenerationModels, BiologicalMorpholinesNADNecrosisOxidantsOxidative StressPoly (ADP-Ribose) Polymerase-1Reactive Oxygen SpeciesRetinal Pigment Epithelium2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneChromonesHydrogen PeroxideMorpholinesNADOxidantsPARP1 protein, humanPoly (ADP-Ribose) Polymerase-1Reactive Oxygen Species

Identifiers

PMID27240523
PMCPMC4886526
OpenAlexW2417257666

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Registered trials

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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.