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

被引:30
作者
Marangoni, Roberta G. [1 ]
Lu, Theresa T. [2 ,3 ]
机构
[1] Northwestern Univ, Feinberg Sch Med, Div Rheumatol, Chicago, IL 60611 USA
[2] Hosp Special Surg, Autoimmun & Inflammat Program & Pediat Rheumatol, 535 East 70th St, New York, NY 10021 USA
[3] Weill Cornell Med Sch, Microbiol & Immunol Dept, New York, NY USA
基金
美国国家卫生研究院;
关键词
dermal white adipose tissue; mesenchymal stromal cells; myofibroblasts; scleroderma; skin fibrosis; MESENCHYMAL STEM-CELLS; PROGRESSIVE SYSTEMIC-SCLEROSIS; STROMAL CELLS; IN-VIVO; REGENERATIVE MEDICINE; NUDE-MICE; MACROPHAGES; ADIPOCYTES; THERAPY; REPAIR;
D O I
10.1097/BOR.0000000000000437
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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.
引用
收藏
页码:585 / 590
页数:6
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