Evidence map›Paper›PMID 26869336›Full record

ArticleAging2016

The signaling pathways by which the Fas/FasL system accelerates oocyte aging.

Jiang Zhu, Fei-Hu Lin, Jie Zhang, Juan Lin, Hong Li, You-Wei Li, Xiu-Wen Tan, Jing-He Tan

Open access · hybridAbstract read
In one paragraph

Article in Aging, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
4.8field-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

16 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Impact of NAD+ metabolism on ovarian aging.Immunity & ageing : I & A · 2023
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Antiaging Effects of Dietary Polysaccharides: Advance and Mechanisms.Oxidative medicine and cellular longevity · 2022
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. 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

8 authors at 2 institutions in 1 country.

Jiang ZhuCollege of Life Science, Northeast Agricultural University, Harbin, 150030, P. R. China.
Fei-Hu LinCollege of Animal Science and Veterinary Medicine, Shandong Agricultural University, Tai-an City 271018, P. R. China.
Jie ZhangCollege of Animal Science and Veterinary Medicine, Shandong Agricultural University, Tai-an City 271018, P. R. China.
Juan LinCollege of Animal Science and Veterinary Medicine, Shandong Agricultural University, Tai-an City 271018, P. R. China.
Hong LiCollege of Animal Science and Veterinary Medicine, Shandong Agricultural University, Tai-an City 271018, P. R. China.
You-Wei LiCollege of Life Science, Northeast Agricultural University, Harbin, 150030, P. R. China.
Xiu-Wen TanCollege of Animal Science and Veterinary Medicine, Shandong Agricultural University, Tai-an City 271018, P. R. China.
Jing-He TanCollege of Life Science, Northeast Agricultural University, Harbin, 150030, P. R. China.
Shandong Agricultural University · CNShanghai Ninth People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In spite of great efforts, the mechanisms for postovulatory oocyte aging are not fully understood. Although our previous work showed that the FasL/Fas signaling facilitated oocyte aging, the intra-oocyte signaling pathways are unknown. Furthermore, the mechanisms by which oxidative stress facilitates oocyte aging and the causal relationship between Ca2+ rises and caspase-3 activation and between the cell cycle and apoptosis during oocyte aging need detailed investigations. Our aim was to address these issues by studying the intra-oocyte signaling pathways for Fas/FasL to accelerate oocyte aging. The results indicated that sFasL released by cumulus cells activated Fas on the oocyte by increasing reactive oxygen species via activating NADPH oxidase. The activated Fas triggered Ca2+ release from the endoplasmic reticulum by activating phospholipase C-γ pathway and cytochrome c pathway. The cytoplasmic Ca2+ rises activated calcium/calmodulin-dependent protein kinase II (CaMKII) and caspase-3. While activated CaMKII increased oocyte susceptibility to activation by inactivating maturation-promoting factor (MPF) through cyclin B degradation, the activated caspase-3 facilitated further Ca2+releasing that activates more caspase-3 leading to oocyte fragmentation. Furthermore, caspase-3 activation and fragmentation were prevented in oocytes with a high MPF activity, suggesting that an oocyte must be in interphase to undergo apoptosis.

Indexed as

AgingAnimalsFas Ligand Proteinfas ReceptorFemaleFluorescent Antibody TechniqueMesothelinMiceOocytesOxidative StressSignal TransductionFas Ligand Proteinfas ReceptorMesothelinMsln protein, mousecaspase-3cytoplasmic Ca2+ risesFas/FasLoocyte agingphospholipase C

Identifiers

PMID26869336
PMCPMC4789583
OpenAlexW2409485268

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.