Evidence map›Paper›PMID 40507871›Full record

ReviewInternational journal of molecular sciences2025

Endometrial Aging and Reproductive Decline: The Central Role of Mitochondrial Dysfunction.

Hiroshi Kobayashi, Miki Nishio, Mai Umetani, Hiroshi Shigetomi, Shogo Imanaka, Hiratsugu Hashimoto

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2025. 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
–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

16 citing papers in PubMed.

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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

6 authors.

Hiroshi KobayashiDepartment of Gynecology and Reproductive Medicine, Ms. Clinic MayOne, 871-1 Shijo-cho, Kashihara 634-0813, Japan.ORCID 0000-0002-8124-6269
Miki NishioDepartment of Gynecology and Reproductive Medicine, Ms. Clinic MayOne, 871-1 Shijo-cho, Kashihara 634-0813, Japan.
Mai UmetaniDepartment of Gynecology and Reproductive Medicine, Ms. Clinic MayOne, 871-1 Shijo-cho, Kashihara 634-0813, Japan.
Hiroshi ShigetomiDepartment of Obstetrics and Gynecology, Nara Medical University, 840 Shijo-cho, Kashihara 634-8522, Japan.
Shogo ImanakaDepartment of Gynecology and Reproductive Medicine, Ms. Clinic MayOne, 871-1 Shijo-cho, Kashihara 634-0813, Japan.
Hiratsugu HashimotoDepartment of Gynecology and Reproductive Medicine, Ms. Clinic MayOne, 871-1 Shijo-cho, Kashihara 634-0813, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Socioeconomic factors have led an increasing number of women to postpone childbirth, thereby elevating the risks of reduced fertility, pregnancy complications, preterm birth, cesarean delivery, and chromosomal abnormalities. While diminished oocyte quality is a well-established contributor to age-related infertility, endometrial dysfunction also plays a pivotal role. Optimizing both oocyte quality and endometrial health is essential for enhancing reproductive outcomes. Although aging has been defined by twelve hallmarks, research specifically addressing age-related changes in endometrial function remains limited. This review examines the process of endometrial aging, with a particular emphasis on mitochondrial function. A comprehensive literature search was conducted using PubMed and Google Scholar to identify relevant studies published up to 31 January 2025. Endometrial aging is driven by multiple biological mechanisms, most notably the decline in endometrial receptivity. Key contributing factors include hormonal dysregulation, chronic inflammation, cell cycle arrest, genomic instability, epigenetic alterations, telomere attrition, and mitochondrial dysfunction. Among these, mitochondrial dysfunction emerges as a central driver of the aging process. Endometrial senescence, precipitated by irreversible mitochondrial impairment, may underlie the progressive decline in reproductive potential. Elucidating the role of mitochondrial dysfunction in aging provides critical insights into the molecular basis of fertility decline, particularly through its impact on endometrial receptivity.

Indexed as

AgingEndometriumMitochondriaReproductionAnimalsCellular SenescenceFemaleHumansInfertility, FemalePregnancyagingendometriumhormonal abnormalitiesmitochondrial dysfunctionmitohormesis

Identifiers

PMID40507871
PMCPMC12154470

What Socratic 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 Socratic graph.