Evidence map›Paper›PMID 41271939›Full record

ArticleScientific reports2025

Amniotic membrane transplantation promotes retinal hole closure in a rabbit model.

Hiroshi Tanaka, Takafumi Miyatani, Takahiro Nakamura, Asako Uehara, Tomoko Horikiri, Yoichiro Shinkai, Kentaro Kojima, Chie Sotozono

Abstract read
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Hiroshi TanakaDepartment of Ophthalmology, Kyoto Prefectural University of Medicine, 465 Kajii-Cho, Hirokoji-Agaru, Kawaramachi-Dori, Kamigyo-Ku, Kyoto, 602-0841, Japan. htanakan@koto.kpu-m.ac.jp.
Takafumi MiyataniDepartment of Ophthalmology, Kyoto Prefectural University of Medicine, 465 Kajii-Cho, Hirokoji-Agaru, Kawaramachi-Dori, Kamigyo-Ku, Kyoto, 602-0841, Japan.
Takahiro NakamuraDepartment of Ophthalmology, Kyoto Prefectural University of Medicine, 465 Kajii-Cho, Hirokoji-Agaru, Kawaramachi-Dori, Kamigyo-Ku, Kyoto, 602-0841, Japan.
Asako UeharaDepartment of Ophthalmology, Kyoto Prefectural University of Medicine, 465 Kajii-Cho, Hirokoji-Agaru, Kawaramachi-Dori, Kamigyo-Ku, Kyoto, 602-0841, Japan.
Tomoko HorikiriDepartment of Ophthalmology, Kyoto Prefectural University of Medicine, 465 Kajii-Cho, Hirokoji-Agaru, Kawaramachi-Dori, Kamigyo-Ku, Kyoto, 602-0841, Japan.
Yoichiro ShinkaiDepartment of Ophthalmology, Kyoto Prefectural University of Medicine, 465 Kajii-Cho, Hirokoji-Agaru, Kawaramachi-Dori, Kamigyo-Ku, Kyoto, 602-0841, Japan.
Kentaro KojimaDepartment of Ophthalmology, Kyoto Prefectural University of Medicine, 465 Kajii-Cho, Hirokoji-Agaru, Kawaramachi-Dori, Kamigyo-Ku, Kyoto, 602-0841, Japan.
Chie SotozonoDepartment of Ophthalmology, Kyoto Prefectural University of Medicine, 465 Kajii-Cho, Hirokoji-Agaru, Kawaramachi-Dori, Kamigyo-Ku, Kyoto, 602-0841, Japan.

Funding

Japan Society for the Promotion of Science 22K16957
6 · The paper itself

Abstract

Amniotic membrane transplantation (AMT) is an effective treatment for refractory macular hole closure, yet the underlying mechanism supporting that effectiveness remains unclear. Here, we investigated the role of retinal regeneration in this process using an in vivo rabbit retinal-hole (RH) model in which AMT was performed on one of the holes. Histological and immunofluorescence examinations with anti-glial fibrillary acidic protein and anti-glutemine synthetase antibodies were conducted to evaluate cell migration and hole closure. Scanning electron microscopy (SEM) and transmission electron microscopy (TEM) were used to analyze the tissues after implantation. Optical coherence tomography scans revealed that AMT promoted RH closure. Histological analyses demonstrated that retinal pigment epithelium (RPE) cells migrated onto the AM, and immunofluorescence analyses showed that retinal glial cells, including Müller cells, contributed to RH closure. SEM and TEM findings revealed cellular coverage and extracellular matrix formation at the AMT site, suggesting successful integration with the surrounding retinal tissue. Furthermore, the loss of mitochondrial cristae within the RPE caused by the creation of RH was suppressed by AMT. In summary, AMT promoted RH closure in a rabbit model by serving as a scaffold for retinal cell migration and by preserving RPE integrity, although regeneration of the retinal-layers was not observed.

Indexed as

AmnionRetinal PerforationsAnimalsCell MovementDisease Models, AnimalEpendymoglial CellsRabbitsRetinaRetinal Pigment EpitheliumTomography, Optical CoherenceAmniotic membraneAmniotic membrane transplantationHuman amniotic membraneMacular holeRetinal hole

Identifiers

PMID41271939
PMCPMC12638848

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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.