Evidence map›Paper›PMID 33107080›Full record

ArticleCell proliferation2021

Involvement of SIRT3-GSK3β deacetylation pathway in the effects of maternal diabetes on oocyte meiosis.

Yongan Xin, Yifei Jin, Juan Ge, Zhenyue Huang, Longsen Han, Congyang Li, Danni Wang, Shuai Zhu, Qiang Wang

Open access · goldAbstract read
In one paragraph

Article in Cell proliferation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

13 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Mitochondrial Calcium Uniporter-Mediated Regulation of the SIRT3/GSK3β/β-Catenin Signaling Pathway in Vascular Remodeling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Mitochondrial Sirtuins in Reproduction.Antioxidants (Basel, Switzerland) · 2021
    Review
  12. Loss of PDK1 Induces Meiotic Defects in Oocytes From Diabetic Mice.Frontiers in cell and developmental biology · 2021
    Article
  13. 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

9 authors at 2 institutions in 1 country.

Yongan XinState Key Laboratory of Reproductive Medicine, Suzhou Municipal Hospital, Nanjing Medical University, Nanjing, China.
Yifei JinSchool of Nursing, Nanjing Medical University, Nanjing, China.
Juan GeState Key Laboratory of Reproductive Medicine, Suzhou Municipal Hospital, Nanjing Medical University, Nanjing, China.
Zhenyue HuangState Key Laboratory of Reproductive Medicine, Suzhou Municipal Hospital, Nanjing Medical University, Nanjing, China.
Longsen HanState Key Laboratory of Reproductive Medicine, Suzhou Municipal Hospital, Nanjing Medical University, Nanjing, China.
Congyang LiState Key Laboratory of Reproductive Medicine, Suzhou Municipal Hospital, Nanjing Medical University, Nanjing, China.
Danni WangState Key Laboratory of Reproductive Medicine, Suzhou Municipal Hospital, Nanjing Medical University, Nanjing, China.
Shuai ZhuState Key Laboratory of Reproductive Medicine, Suzhou Municipal Hospital, Nanjing Medical University, Nanjing, China.
Qiang WangState Key Laboratory of Reproductive Medicine, Suzhou Municipal Hospital, Nanjing Medical University, Nanjing, China.ORCID https://orcid.org/0000-0003-0000-9139
Suzhou Municipal Hospital · CNNanjing Medical University · CN

Funding

National Key Scientific Research Projects 2018YFC1004000National Natural Science Foundation of China 31771657National Natural Science Foundation of China 81925014Science Foundation for Distinguished Young Scholars of Jiangsu Province BK20180035
6 · The paper itself

Abstract

objectivesIt has been widely reported that maternal diabetes impairs oocyte quality. However, the responsible mechanisms remain to be explored. In the present study, we focused on whether SIRT3-GSK3β pathway mediates the meiotic defects in oocytes from diabetic mice. MATERIALS AND

methodsGSK3β functions in mouse oocyte meiosis were first detected by targeted siRNA knockdown. Spindle assembly and chromosome alignment were visualized by immunostaining and analysed under the confocal microscope. PCR-based site mutation of specific GSK3β lysine residues was used to confirm which lysine residues function in oocyte meiosis. siRNA knockdown coupled with cRNA overexpression was performed to detect SIRT3-GSK3β pathway functions in oocyte meiosis. Immunofluorescence was performed to detect ROS levels. T1DM mouse models were induced by a single intraperitoneal injection of streptozotocin.

resultsIn the present study, we found that specific depletion of GSK3β disrupts maturational progression and meiotic apparatus in mouse oocytes. By constructing site-specific mutants, we further revealed that acetylation state of lysine (K) 15 on GSK3β is essential for spindle assembly and chromosome alignment during oocyte meiosis. Moreover, non-acetylation-mimetic mutant GSK3β-K15R is capable of partly preventing the spindle/chromosome anomalies in oocytes with SIRT3 knockdown. A significant reduction in SIRT3 protein was detected in oocytes from diabetic mice. Of note, forced expression of GSK3β-K15R ameliorates maternal diabetes-associated meiotic defects in mouse oocytes, with no evident effects on oxidative stress.

conclusionOur data identify GSK3β as a cytoskeletal regulator that is required for the assembly of meiotic apparatus, and discover a beneficial effect of SIRT3-dependent GSK3β deacetylation on oocyte quality from diabetic mice.

Indexed as

MeiosisAcetylationAnimalsCells, CulturedDiabetes Mellitus, ExperimentalFemaleGlycogen Synthase Kinase 3 betaInjections, IntraperitonealMiceMice, Inbred ICROocytesSirtuin 3StreptozocinGlycogen Synthase Kinase 3 betaGsk3b protein, mouseSirt3 protein, mouseSirtuin 3Streptozocindiabetesmeiosisoocyteoxidative stressSirtuin

Identifiers

PMID33107080
PMCPMC7791178
OpenAlexW3094307759

What OpenQuestion holds

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LicenceCC BY
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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.