Early Angiogenesis-Dependent CXCL12 Attracts Adipose-Derived Stem Cells to Promote the Repair of Fat Grafting in a Mouse Model.

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• 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

Abstract (original English)

The unpredictable and unstable tissue retention rate of autologous fat grafting remains an obstacle faced by plastic surgeons. The authors' previous study using a fat grafting mouse model with donor sites showed that adipose-derived stem cell (ASC) infiltration in the recipient site was delayed, leading to poor regeneration and lower retention. Thus, the mechanism behind the differential infiltration of ASCs needed to be explored. First, the authors locally injected C-X-C chemokine ligand 12 (CXCL12) or C-X-C motif chemokine receptor 4 (CXCR4) inhibitor AMD3100 in the recipient or donor site, respectively (CXCL12 + AMD3100 - , CXCL12 - AMD3100 + , and CXCL12 + AMD3100 + groups). The authors compared the migration of ASCs, adipose regeneration, and long-term retention. Next, the authors explored the role of angiogenesis using a normal/ischemic mice model in which the authors test the expression of CXCL12/CXCR4, migration of ASCs, and adipose regeneration. Blocking CXCL12 in the donor site using AMD3100 (CXCL12 - AMD3100 + and CXCL12+AMD3100+ groups) could accelerate ASC infiltration and promote adipose regeneration and long-term retention ( P < 0.05) compared with the other groups. CXCL12 and its receptor CXCR4 were more highly expressed in normal than in ischemic adipose tissue; consistently, there were more ASCs infiltrating normal than ischemic adipose tissue early after surg

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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