Removing Lipid Droplets Improves Fat Transplantation Outcomes in a Mouse Model through Suppressing Pro-fibrotic Macrophage Responses.

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 clinical efficacy and predictability of autologous fat grafting are frequently undermined by uncontrolled fibrosis and oil cyst formation. While lipid droplets (LDs) metabolic imbalance is recognized as a critical factor influencing graft outcomes, the underlying mechanisms linking LDs to adverse tissue remodeling remain poorly understood. This study aimed to elucidate the mechanistic impact of extracellular LDs on fat graft outcomes in a murine model, with a specific focus on their role in modulating macrophage-mediated inflammation and fibrosis. Fat grafts were transplanted into C57BL/6J mice and divided into two groups: an oil-retained group (control) and an oil-removed group (intervention). Grafts were harvested at serial timepoints (2-12 weeks) for comprehensive analysis, including histopathology (H&E, Masson's trichrome), quantitative PCR for inflammatory and fibrotic markers (TNF-α, IL-1β, IL-6, TGF-β), and immunofluorescence staining to assess macrophage polarization (CD86 for M1, CD206 for M2). The presence of excess extracellular LDs acted as a potent inflammatory trigger, driving a significant upregulation of pro-inflammatory cytokines, including TNF-α (2.4-fold), IL-6 (1.9-fold), and IL-1β (2.8-fold). This pro-inflammatory microenvironment was associated with a dominant M1 macrophage phenotype. Conversely, the preoperative removal of LDs fundamentally altered th

Evidence level

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

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