Kewei Chen
Researcher in plastic surgery at Wenzhou Medical University and first author of a mouse study on engineered stem-cell exosomes that speed wound healing by changing fibroblast metabolism
Department of Plastic Surgery, The First Affiliated Hospital of Wenzhou Medical University (2026, at the time of the study)
Chronic wounds, such as foot ulcers in people with diabetes, can stay open for months. In the Atlas study CHEN2026 in Cellular Signalling, Kewei Chen was first author. The team engineered adipose-derived stem cells, stem cells taken from fat tissue, so that the tiny vesicles they release (exosomes) carried FGF21, a hormone that affects energy use. When these exosomes were given to skin fibroblasts, the cells that rebuild tissue, the fibroblasts switched up glycolysis, the quick sugar-burning pathway, with the energy sensor AMPK turned on and mTOR signalling turned down. The fibroblasts divided and moved faster, and wounds in a mouse model closed sooner. The evidence comes from cells and mice.
PubMed lists Chen in the Department of Plastic Surgery at the First Affiliated Hospital of Wenzhou Medical University, with Li L as senior author. Because the name is very common, no other paper could be tied to this person with confidence, and no official profile page was found.
Milestones in the Atlas
A selection, not a full bibliography: only papers that meet the Atlas inclusion criteria.
| Year | Evidence | Study |
|---|---|---|
| 2026 | A | FGF21-modified adipose stem cell-derived exosomes promote wound healing by activating fibroblast glycolysis through AMPK/mTOR signaling. CHEN2026 First author: showed in fibroblasts and a mouse wound model that FGF21-loaded stem-cell exosomes boost glycolysis, activate AMPK, lower mTOR signalling and speed wound closure. |
Co-authors in the Atlas 1
People with a profile here who share at least one study with Kewei Chen.
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- Wanying Chen Member of a Wenzhou wound-healing and adipose-stem-cell research group who contributed to a study of FGF21-modified exosomes that promote wound healing through AMPK–mTOR
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