Evidence map›Paper›PMID 35631296›Full record

ArticleNutrients2022

Trehalose Suppresses Lysosomal Anomalies in Supporting Cells of Oocytes and Maintains Female Fertility.

Woojin Kang, Eri Ishida, Mitsuyoshi Amita, Kuniko Tatsumi, Hitomi Yonezawa, Miku Yohtsu, Daiki Katano, Kae Onozawa, Erika Kaneko, Wakako Iwasaki and 8 more

Open access · goldAbstract read
In one paragraph

Article in Nutrients, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.6field-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

6 citing papers in PubMed, 8 citations in OpenAlex.

  1. Trehalose's untapped mechanisms in alzheimer's: gut-brain-autophagy signalling beyond the usual targets.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2026
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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

18 authors at 3 institutions in 1 country.

Woojin KangDivision of Reproductive Medicine, Center of Maternal-Fetal, Neonatal and Reproductive Medicine, National Center for Child Health and Development, 2-10-1 Okura, Setagaya, Tokyo 157-8535, Japan.
Eri IshidaDivision of Reproductive Medicine, Center of Maternal-Fetal, Neonatal and Reproductive Medicine, National Center for Child Health and Development, 2-10-1 Okura, Setagaya, Tokyo 157-8535, Japan.
Mitsuyoshi AmitaDivision of Reproductive Medicine, Center of Maternal-Fetal, Neonatal and Reproductive Medicine, National Center for Child Health and Development, 2-10-1 Okura, Setagaya, Tokyo 157-8535, Japan.
Kuniko TatsumiDivision of Reproductive Medicine, Center of Maternal-Fetal, Neonatal and Reproductive Medicine, National Center for Child Health and Development, 2-10-1 Okura, Setagaya, Tokyo 157-8535, Japan.
Hitomi YonezawaDepartment of Life Sciences, School of Agriculture, Meiji University, 1-1-1 Higashi-Mita, Kawasaki, Kanagawa 214-8571, Japan.
Miku YohtsuDepartment of Life Sciences, School of Agriculture, Meiji University, 1-1-1 Higashi-Mita, Kawasaki, Kanagawa 214-8571, Japan.
Daiki KatanoDepartment of Reproductive Biology, National Research Institute for Child Health and Development, 2-10-1, Okura, Setagaya, Tokyo 157-8535, Japan.
Kae OnozawaDivision of Reproductive Medicine, Center of Maternal-Fetal, Neonatal and Reproductive Medicine, National Center for Child Health and Development, 2-10-1 Okura, Setagaya, Tokyo 157-8535, Japan.
Erika KanekoDivision of Reproductive Medicine, Center of Maternal-Fetal, Neonatal and Reproductive Medicine, National Center for Child Health and Development, 2-10-1 Okura, Setagaya, Tokyo 157-8535, Japan.
Wakako IwasakiDivision of Reproductive Medicine, Center of Maternal-Fetal, Neonatal and Reproductive Medicine, National Center for Child Health and Development, 2-10-1 Okura, Setagaya, Tokyo 157-8535, Japan.
Natsuko NaitoDivision of Reproductive Medicine, Center of Maternal-Fetal, Neonatal and Reproductive Medicine, National Center for Child Health and Development, 2-10-1 Okura, Setagaya, Tokyo 157-8535, Japan.
Mitsutoshi YamadaDepartment of Obstetrics and Gynecology, Keio University School of Medicine, 35 Shinanomachi, Shinjuku, Tokyo 160-8582, Japan.ORCID 0000-0002-7560-316X
Natsuko KawanoDepartment of Life Sciences, School of Agriculture, Meiji University, 1-1-1 Higashi-Mita, Kawasaki, Kanagawa 214-8571, Japan.
Mami MiyadoDepartment of Food and Nutrition, Beppu University, 82 Kita-Ishigaki, Beppu, Oita 874-8501, Japan.
Ban SatoDepartment of Life Sciences, School of Agriculture, Meiji University, 1-1-1 Higashi-Mita, Kawasaki, Kanagawa 214-8571, Japan.
Hidekazu SaitoDivision of Reproductive Medicine, Center of Maternal-Fetal, Neonatal and Reproductive Medicine, National Center for Child Health and Development, 2-10-1 Okura, Setagaya, Tokyo 157-8535, Japan.
Takakazu SaitoDivision of Reproductive Medicine, Center of Maternal-Fetal, Neonatal and Reproductive Medicine, National Center for Child Health and Development, 2-10-1 Okura, Setagaya, Tokyo 157-8535, Japan.
Kenji MiyadoDepartment of Reproductive Biology, National Research Institute for Child Health and Development, 2-10-1, Okura, Setagaya, Tokyo 157-8535, Japan.ORCID 0000-0002-8339-6738
National Center For Child Health and Development · JPMeiji University · JPKeio University Hospital · JP

Funding

JSPS KAKENHI JP19H01067JSPS KAKENHI JP19K09793
6 · The paper itself

Abstract

Supporting cells of oocytes, i.e., cumulus cells, control oocyte quality, which determines fertilization success. Therefore, the transformation of mature and immature cumulus cells (MCCs and ICCs, respectively) into dysmature cumulus cells (DCCs) with dead characteristics deteriorates oocyte quality. However, the molecular basis for this transformation remains unclear. Here, we explored the link between autophagic decline and cumulus transformation using cumulus cells from patients with infertility, female mice, and human granulosa cell-derived KGN cell lines. When human cumulus cells were labeled with LysoTracker probes, fluorescence corresponding to lysosomes was enhanced in DCCs compared to that in MCCs and ICCs. Similarly, treatment with the autophagy inhibitor chloroquine elevated LysoTracker fluorescence in both mouse cumulus cells and KGN cells, subsequently suppressing ovulation in female mice. Electron microscopy analysis revealed the proliferation of abnormal lysosomes in chloroquine-treated KGN cells. Conversely, the addition of an autophagy inducer, trehalose, suppressed chloroquine-driven problematic lysosomal anomalies and ameliorated ovulation problems. Our results suggest that autophagy maintains the healthy state of the supporting cells of human oocytes by suppressing the formation of lysosomes. Thus, our results provide insights into the therapeutic effects of trehalose on female fertility.

Indexed as

OocytesTrehaloseAnimalsChloroquineFemaleFertilityHumansLysosomesMiceChloroquineTrehaloseautophagychloroquinelysosomal anomaliesoocyte qualitytrehalose

Identifiers

PMID35631296
PMCPMC9148094
OpenAlexW4281259086

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.