Dihydromyricetin attenuates fibrosis-associated features of hypertrophic scar with accompanying changes in PI3K/AKT/mTOR-related signaling.
What this study shows
Dihydromyricetin reduced collagen I/III and α-SMA in hypertrophic scar fibroblasts and improved scar elevation in a rabbit ear model, with accompanying reductions in AKT and mTOR phosphorylation; causality was not established.
At a glance
| Evidence type | A Animal model Marked A because it is an animal intervention or observation study measuring an organismal outcome (model: Rabbit ear hypertrophic scar model; human hypertrophic scar fibroblasts); the code names the system studied -- animal work can be rigorous and still not be human data. |
| Study type | 4 - Animal Study |
| Model system | Rabbit ear hypertrophic scar model; human hypertrophic scar fibroblasts |
| Journal | Frontiers in Pharmacology |
| Year | 2026 |
| Peer reviewed | Yes |
| Record last updated | 2026-10-01 |
| Source | DOI 10.3389/fphar.2026.1862651 · PMID 42656474 · Free full text (PMC13506778) |
Extracted findings
These fields were extracted from the paper with AI assistance and have not been checked against the source. Read them as a pointer into the paper, not as curated claims; where they disagree with the curated summary above, the curated summary stands.
| Intervention | Dihydromyricetin; LY294002 (PI3K inhibitor) |
| Target | PI3K/AKT/mTOR; AKT1 |
| Model | Rabbit; human fibroblasts |
| Effect | Reduced fibrotic marker expression and scar elevation index; decreased AKT and mTOR phosphorylation |
In the Atlas
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