ACE2 Inhibits Dermal Regeneration Through Ang II in Tissue Expansion
Bai R., Liang B., Guo Y., Liu W., Wen Z., Wang Z.
Prospective Study, published in J Cosmet Dermatol (2025) — summary generated from the PubMed abstract.
Early human evidence such as case series or small samples is exploring possible benefits.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Prospective Study
- Journal
- J Cosmet Dermatol (2025)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 39829293
- PMCID
- PMC11744341
- DOI
- 10.1111/jocd.16767
Abstract (original English)
Background Tissue expansion is a widely employed technique in reconstructive surgery aimed at addressing considerable skin defects. Nevertheless, matters like inadequate expansion capability and the potential for skin breakage due to the fragility of the expanded tissue present notable hurdles in enhancing skin regeneration during this process. Angiotensin-converting enzyme 2 (ACE2) is recognized for its essential role in facilitating tissue renewal and regeneration. However, its precise impact on skin renewal during tissue expansion remains underexplored. This study seeks to elucidate ACE2's contribution to skin regeneration, specifically examining its role in collagen synthesis. Methods This study evaluated the expression and distribution of ACE2 in expanded skin using samples derived from both rats and human patients. Additionally, we investigated ACE2 expression in stretched keratinocytes in vitro. ACE2 knockout keratinocytes were transfected with small interfering RNA (siRNA) and cocultured with fibroblasts to observe fibroblast proliferation and migration. MLN-4760 was utilized to inhibit the ACE2 enzymatic activity. Additionally, we analyzed parameters such as the size of expanded skin, dermal thickness, and the levels of collagen I (COL I), collagen III (COL III), and transforming growth factor β (TGF-β) to elucidate the role of ACE2 in the context of expanded skin. Res
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
Evidence level
Early human evidence such as case series or small samples is exploring possible benefits.
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