Evidence map›Paper›PMID 40915932›Full record

ArticleExperimental animals2026

D-galactose treatment accumulates AGEs but induces no further detrimental effects in HR-1 mouse skin.

Mako Isemura, Ryoga Kinosita, Sakura Hattori, Karina Kouzaki, Yuki Tamura, Hiroya Urabe, Hiroyuki Uno, Ryuji Akimoto, Koichi Nakazato

Abstract read
In one paragraph

Article in Experimental animals, 2026. 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

9 authors.

Mako IsemuraHOMER ION Laboratory Co., Ltd., Shinsen 17-2, Shibuya-Ku, Tokyo 150-0045, Japan.
Ryoga KinositaNippon Sport Science University, 7-1-1 Fukazawa, Setagaya-Ku, Tokyo 158-8508, Japan.
Sakura HattoriNippon Sport Science University, 7-1-1 Fukazawa, Setagaya-Ku, Tokyo 158-8508, Japan.
Karina KouzakiNippon Sport Science University, 7-1-1 Fukazawa, Setagaya-Ku, Tokyo 158-8508, Japan.
Yuki TamuraNippon Sport Science University, 7-1-1 Fukazawa, Setagaya-Ku, Tokyo 158-8508, Japan.
Hiroya UrabeHOMER ION Laboratory Co., Ltd., Shinsen 17-2, Shibuya-Ku, Tokyo 150-0045, Japan.
Hiroyuki UnoHOMER ION Laboratory Co., Ltd., Shinsen 17-2, Shibuya-Ku, Tokyo 150-0045, Japan.
Ryuji AkimotoHOMER ION Laboratory Co., Ltd., Shinsen 17-2, Shibuya-Ku, Tokyo 150-0045, Japan.
Koichi NakazatoNippon Sport Science University, 7-1-1 Fukazawa, Setagaya-Ku, Tokyo 158-8508, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

As aging affects the appearance of the skin, anti-aging research has intensified in dermatology, skincare, and aesthetic medicine. Because natural aging takes a very long time, one essential anti-aging approach is to pharmacologically mimic aging, such as with D-galactose treatment. Hairless mice (HR-1) have been extensively used in skin research because of their lack of body hair and ease of animal care. In the present study, HR-1 mice were treated with D-galactose to determine whether detrimental effects were induced in the skin. After 3 months of D-galactose treatment, AGEs in the skin significantly increased. On the other hand, no signs of skin disorders (dermal thickness, type I collagen content, expression of various genes, collagen synthesis, and degradation signals) were observed. Even when the concentration of D-galactose increased, no apparent changes in dermal thickness were observed. These findings suggest that D-galactose treatment induces AGEs accumulation but no further detrimental effects in the HR-1 skin.

Indexed as

AgingGalactoseGlycation End Products, AdvancedSkinSkin AgingAnimalsCollagen Type IFemaleMaleMiceMice, HairlessCollagen Type IGalactoseGlycation End Products, AdvancedD-galactosehairless miceskin aging

Identifiers

PMID40915932
PMCPMC12826573

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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.