Evidence map›Paper›PMID 41457116›Full record

ArticleJournal of assisted reproduction and genetics2026

Functional interplay between endoplasmic reticulum stress and mitochondrial activity in a post-ovulatory aging model of mouse oocytes.

Fumihiro Nakamura, Isao Takehara, Saki Hine, Midori Saito, Jun Matsukawa, Michi Nishi, Satoru Nagase

Abstract read
In one paragraph

Article in Journal of assisted reproduction and genetics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

7 authors.

Fumihiro NakamuraDepartment of Obstetrics and Gynecology, Faculty of Medicine, Yamagata University, 2-2-2, Iida-Nishi, Yamagata, 990-9585, Japan.
Isao TakeharaDepartment of Obstetrics and Gynecology, Faculty of Medicine, Yamagata University, 2-2-2, Iida-Nishi, Yamagata, 990-9585, Japan. i-takehara@med.id.yamagata-u.ac.jp.ORCID http://orcid.org/0009-0004-4406-859X
Saki HineDepartment of Obstetrics and Gynecology, Faculty of Medicine, Yamagata University, 2-2-2, Iida-Nishi, Yamagata, 990-9585, Japan.
Midori SaitoDepartment of Obstetrics and Gynecology, Faculty of Medicine, Yamagata University, 2-2-2, Iida-Nishi, Yamagata, 990-9585, Japan.
Jun MatsukawaDepartment of Obstetrics and Gynecology, Faculty of Medicine, Yamagata University, 2-2-2, Iida-Nishi, Yamagata, 990-9585, Japan.
Michi NishiDepartment of Obstetrics and Gynecology, Faculty of Medicine, Yamagata University, 2-2-2, Iida-Nishi, Yamagata, 990-9585, Japan.
Satoru NagaseDepartment of Obstetrics and Gynecology, Faculty of Medicine, Yamagata University, 2-2-2, Iida-Nishi, Yamagata, 990-9585, Japan.

Funding

Japan Society for the Promotion of Science 21K16805
6 · The paper itself

Abstract

purposeTo investigate whether targeting the ER-mitochondria axis can improve embryonic development in a post-ovulatory aging (POA) model by evaluating organelle-specific modulation.

methodsFresh oocytes were collected immediately after ovulation, and post-ovulatory aged oocytes were obtained using a mouse model. Fresh oocytes were treated with thapsigargin (an ER stress inducer) or CCCP (a mitochondrial inhibitor), and ER stress (GRP78 fluorescence) and mitochondrial superoxide status (MitoSOX™ fluorescence) were assessed. Aged oocytes were treated with salubrinal (an ER stress modulator), 5-aminolevulinic acid (5-ALA, a mitochondrial modulator), or both. Embryonic development was evaluated via blastocyst formation and cell death rates.

resultsIn fresh oocytes, CCCP increased GRP78 fluorescence, and thapsigargin increased MitoSOX fluorescence, consistent with bidirectional ER-mitochondria stress propagation. In POA oocytes, salubrinal reduced GRP78 fluorescence but not MitoSOX, whereas 5-ALA reduced MitoSOX fluorescence but not GRP78; the combined treatment showed no additive effects on either proxy marker. Despite the lack of additivity at the marker level, blastocyst formation increased and apoptosis decreased in all treatment groups, with no additional benefit of combined treatment compared with single agents.

conclusionsIn this POA model, ER-mitochondria coupling detected in freshly ovulated oocytes appeared attenuated. While our single-marker readouts (GRP78 and MitoSOX) are limited proxies, independent targeting of either organelle modestly improved blastocyst formation. These data support a hypothesis-generating framework for future studies in maternal aging models. Results were obtained under 20% O₂ culture and may be conservative relative to physiologic (5%) O₂ conditions.

Indexed as

AgingEndoplasmic Reticulum StressMitochondriaOocytesAnimalsApoptosisBlastocystCarbonyl Cyanide m-Chlorophenyl HydrazoneCellular SenescenceCinnamatesEmbryonic DevelopmentEndoplasmic Reticulum Chaperone BiPFemaleMiceOvulationThapsigarginCarbonyl Cyanide m-Chlorophenyl HydrazoneCinnamatesEndoplasmic Reticulum Chaperone BiPHspa5 protein, mousesalubrinalThapsigarginThioureaARTBlastocyst formationER stressMitochondrial dysfunctionOocyte aging

Identifiers

PMID41457116
PMCPMC12982706

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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.