Evidence map›Paper›PMID 42656474›Full record

ArticleFrontiers in pharmacology2026

Dihydromyricetin attenuates fibrosis-associated features of hypertrophic scar with accompanying changes in PI3K/AKT/mTOR-related signaling.

Peng Cao, Ao Shi, Yunwei Wang, Shuoyi Hui, Guozhong Lyu

Abstract read
In one paragraph

Article in Frontiers in pharmacology, 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
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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

5 authors.

Peng Cao *Burn & Trauma Treatment Center, Affiliated Hospital of Jiangnan University, Wuxi, China.
Ao Shi *Department of Burn Plastic and Wound Repair Surgery, The Second Hospital of Lanzhou University, Lanzhou, China.
Yunwei Wang *Department of Burn Plastic and Wound Repair Surgery, The Second Hospital of Lanzhou University, Lanzhou, China.
Shuoyi HuiDepartment of Orthodontics, State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi Key Laboratory of Orthodontics, School of Stomatology, The Fourth Military Medical University, Xi'an, China.
Guozhong LyuBurn & Trauma Treatment Center, Affiliated Hospital of Jiangnan University, Wuxi, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study investigated whether dihydromyricetin (DHM) attenuates fibrosis-associated features in hypertrophic scar (HS) and whether these effects are accompanied by changes in PI3K/AKT/mTOR-related signaling. Network pharmacology identified overlapping targets between DHM and HS, and subsequent protein-protein interaction and enrichment analyses highlighted AKT1 as a candidate hub target potentially associated with PI3K/AKT/mTOR-related signaling. Molecular docking and 50-ns molecular dynamics simulation further indicated a stable predicted interaction pattern between DHM and AKT1. For experimental validation, hypertrophic scar tissues, paired normal skin tissues, hypertrophic scar fibroblasts (HSFs), and paired normal skin fibroblasts (NSFs) were examined. Compared with paired normal controls, HS tissues and HSFs showed increased expression of collagen I, collagen III, and α-SMA. Untreated HSFs also exhibited higher basal p-AKT/AKT and p-mTOR/mTOR ratios than paired NSFs. In HSFs, DHM reduced the CCK-8 viability signal and the expression of fibrosis-related markers, and these changes were accompanied by decreased phosphorylation of AKT and mTOR. Live/dead staining did not show an obvious increase in PI-positive dead cells after 15 μM DHM treatment, suggesting that the decrease in CCK-8 signal may reflect reduced metabolic activity and growth inhibition rather than extensive acute cell death. Treatment with LY294002 alone and combined treatment with DHM and LY294002 further supported the involvement of PI3K/AKT/mTOR-related signaling in the regulation of fibrosis-associated features in HSFs. In a rabbit ear hypertrophic scar model, DHM improved gross scar appearance, reduced the scar elevation index, decreased the collagen-positive area fraction in Masson's trichrome-stained sections, and alleviated histopathological alterations. Together, these findings indicate that DHM attenuated fibrosis-associated features of HS

Indexed as

dihydromyricetinfibrosishypertrophic scarhypertrophic scar fibroblastsnetwork pharmacologyPI3K/AKT/mTOR signaling

Identifiers

PMID42656474
PMCPMC13506778

What Socratic holds

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Read underepoch 390

Registered trials

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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 Socratic graph.