The roles of dermal white adipose tissue loss in scleroderma skin fibrosis.

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)

Purpose of review Dermal white adipose tissue (DWAT) is distinct from subcutaneous white adipose tissue and is lost in scleroderma skin fibrosis. The roles of DWAT loss in scleroderma skin fibrosis have not been well understood, and here we discuss recent findings that begin to provide insight into the multiple mechanisms involved. Recent findings The DWAT loss in part reflects the direct contribution of DWAT cells to the fibrotic tissue, with the reprogramming of adipocytes to myofibroblasts. The DWAT contains reparative adipose-derived stromal cells and expresses antifibrotic cytokines such as adiponectin, and the loss of these skin-protective mechanisms with DWAT loss further contributes to skin fibrosis and injury. Summary Potentially, halting or reversing the transdifferentiation of adipocytes to myofibroblasts along with improving survival of reparative adipose-derived stromal cells (ADSCs) and expression of antifibrotic cytokines may be effective therapeutic avenues.

Evidence level

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

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