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

Area of Science:

• Dermatology
• Adipose Tissue Biology
• Fibrosis Research

Background:

• Dermal white adipose tissue (DWAT) is a distinct fat depot with unique properties.
• DWAT is significantly reduced in scleroderma, a fibrotic skin disease.
• The precise roles of DWAT loss in scleroderma pathogenesis remain incompletely understood.

Purpose of the Study:

• To review recent findings elucidating the mechanisms by which DWAT loss contributes to scleroderma skin fibrosis.
• To explore the functional implications of DWAT alterations in the context of fibrotic skin injury.

Main Methods:

• Review of current literature on DWAT, scleroderma, and fibrosis.
• Analysis of cellular and molecular mechanisms involved in DWAT loss and its consequences.
• Synthesis of findings to understand the interplay between DWAT and fibrotic processes.

Main Results:

• DWAT loss in scleroderma involves the direct contribution of adipocytes, which transdifferentiate into myofibroblasts.
• The depletion of reparative adipose-derived stromal cells (ADSCs) within DWAT diminishes protective functions.
• Reduced expression of antifibrotic cytokines, such as adiponectin, exacerbates skin fibrosis and injury.

Conclusions:

• Therapeutic strategies could target the reversal of adipocyte-to-myofibroblast transdifferentiation.
• Enhancing the survival and function of ADSCs represents a potential treatment avenue.
• Restoring antifibrotic cytokine expression may mitigate skin fibrosis in scleroderma.