Evidence map›Paper›PMID 25633094›Full record

ArticleMolecular neurobiology2016

GOLPH3 Mediated Golgi Stress Response in Modulating N2A Cell Death upon Oxygen-Glucose Deprivation and Reoxygenation Injury.

Ting Li, Hong You, Xiaoye Mo, Wenfang He, Xiangqi Tang, Zheng Jiang, Shiyu Chen, Yang Chen, Jie Zhang, Zhiping Hu

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% 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, 1 synthesis or guideline pooled it, 76 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Oxidative Stress and Ginsenosides: An Update on the Molecular Mechanisms.Oxidative medicine and cellular longevity · 2022
    Review
  18. Review
  19. Article
  20. The role of the Golgi apparatus in disease (Review).International journal of molecular medicine · 2021
    Review
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

10 authors at 2 institutions in 1 country.

Ting LiThe Second Xiangya Hospital Central South University, Changsha, Hunan, China.
Hong YouThe Second Xiangya Hospital Central South University, Changsha, Hunan, China.
Xiaoye MoThe Second Xiangya Hospital Central South University, Changsha, Hunan, China.
Wenfang HeThe Second Xiangya Hospital Central South University, Changsha, Hunan, China.
Xiangqi TangThe Second Xiangya Hospital Central South University, Changsha, Hunan, China.
Zheng JiangThe Second Xiangya Hospital Central South University, Changsha, Hunan, China.
Shiyu ChenThe Second Xiangya Hospital Central South University, Changsha, Hunan, China.
Yang ChenThe Second Xiangya Hospital Central South University, Changsha, Hunan, China.
Jie ZhangThe Second Xiangya Hospital Central South University, Changsha, Hunan, China. lilisten2011@163.com.
Zhiping HuThe Second Xiangya Hospital Central South University, Changsha, Hunan, China. huzhipingxy@gmail.com.
Central South University · CNSecond Xiangya Hospital of Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Increasing evidence implicating that the organelle-dependent initiation of cell death merits further research. The evidence also implicates Golgi as a sensor and common downstream-effector of stress signals in cell death pathways, and it undergoes disassembly and fragmentation during apoptosis in several neurological disorders. It has also been reported that during apoptotic cell death, there is a cross talk between ER, mitochondria, and Golgi. Thus, we hypothesized that Golgi might trigger death signals during oxidative stress through its own machinery. The current study found that GOLPH3, an outer membrane protein of the Golgi complex, was significantly upregulated in N2A cells upon oxygen-glucose deprivation and reoxygenation (OGD/R), positioning from the compact perinuclear ribbon to dispersed vesicle-like structures throughout the cytoplasm. Additionally, elevated GOLPH3 promoted a stress-induced conversion of the LC3 subunit I to II and reactive oxygen species (ROS) production in long-term OGD/R groups. The collective data indicated that GOLPH3 not only acted as a sensor of Golgi stress for its prompt upregulation during oxidative stress but also as an initiator that triggered and propagated specific Golgi stress signals to downstream effectors. This affected ROS production and stress-related autophagy and finally controlled the entry into apoptosis. The data also supported the hypothesis that the Golgi apparatus could be an ideal target for stroke, neurodegenerative diseases, or cancer therapy through its own functional proteins.

Indexed as

Stress, PhysiologicalAnimalsCell DeathCell LineDisease Models, AnimalDown-RegulationGlucoseGolgi ApparatusIntracellular SpaceMiceOxygenPhosphoproteinsReactive Oxygen SpeciesTime FactorsGlucoseGPP34 protein, mouseOxygenPhosphoproteinsReactive Oxygen SpeciesApoptosisAutophagyER stressGolgi stress responseGOLPH3Ischemia/reperfusionMitochondriaOxidative stressOxygen-glucose deprivation and reoxygenation (OGD/R)Reactive oxygen species (ROS)

Identifiers

PMID25633094
OpenAlexW2016697747

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.