Eliminación de gotitas lipídicas mejora los resultados del trasplante de grasa en un modelo de ratón al suprimir las...

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 this response. The oil-removed group exhibited markedly superior outcomes, including a 1.25-fold greater volume retention (p < 0.01) and a 60% reduction in oil cyst area (p < 0.01) at 12 weeks. Mechanistically, these improvements were linked to a decisive shift in macrophage polarization toward a pro-regenerative M2 phenotype, as evidenced by a significantly higher CD206+/CD86+ cell ratio (1.76 vs. 0.86 in controls).

LDs overload exacerbated graft failure through M1 macrophage-mediated chronic inflammation and pathological fibrosis. Preoperative removal of these lipid droplets mitigates this detrimental inflammatory cascade, improves graft retention, and represents a critical and actionable strategy for enhancing the outcomes of clinical fat transplantation.

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