Subcutaneous fat transplantation improves dermal adipose dysfunction by regulating autophagy and mitophagy

Abstract

Background

Dermal white adipose tissue (dWAT) plays a crucial role in maintaining skin structure and functional homeostasis. Dysfunction of dWAT is closely associated with skin aging and fibrosis, with the impairment of autophagy and mitophagy considered the key mechanisms underlying adipose tissue dysfunction. Autologous fat transplantation (AFT) is widely used in plastic and aesthetic surgeries; however, its effects on dermal adipose function remain unclear.

Methods

In this study, a mouse model of dermal adipose dysfunction was established using the PPAR-γ inhibitor GW9662, followed by subcutaneous AFT. Dermal adipose thickness, lipid metabolism, autophagy, and mitophagy-related protein expression (PPAR-γ, PLIN-1, Beclin-1, LC3, Pink-1, and Parkin) were analyzed by H&E staining, immunohistochemistry, and qRT-PCR.

Results

GW9662 treatment significantly inhibited lipid metabolism and reduced the expression of autophagy- and mitophagy-related markers, indicating a possible impairment in these pathways. AFT upregulated these markers, suggesting a potential modulatory effect on autophagy and mitophagy.

Conclusion

Dermal adipose dysfunction induced by PPAR-γ inhibition may involve dysregulation of autophagy and mitophagy. Subcutaneous fat transplantation appeared to partially reverse these molecular alterations, thereby supporting its potential application in skin aging and adipose tissue restoration.