Roberta G Marangoni1, Theresa T Lu. 1. aDivision of Rheumatology, Northwestern University Feinberg School of Medicine, Chicago, Illinois bAutoimmunity and Inflammation Program and Pediatric Rheumatology, Hospital for Special Surgery cMicrobiology and Immunology Department, Weill Cornell Medical School, New York, New York, USA.
Abstract
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.
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.
Authors: Manja Newe; Theresa A Kant; Maximilian Hoffmann; Johanna S E Rausch; Luise Winter; Karolina Künzel; Erik Klapproth; Claudia Günther; Stephan R Künzel Journal: Naunyn Schmiedebergs Arch Pharmacol Date: 2021-08-19 Impact factor: 3.195
Authors: William D Shipman; Marvin J Sandoval; Keila Veiga; Laura T Donlin; Theresa T Lu Journal: Curr Opin Immunol Date: 2020-05-05 Impact factor: 7.486
Authors: Anne M Stevens; Kathryn S Torok; Suzanne C Li; Sarah F Taber; Theresa T Lu; Francesco Zulian Journal: Front Immunol Date: 2019-06-25 Impact factor: 7.561
Authors: Benjamin Korman; Roberta Goncalves Marangoni; Gabriel Lord; Jerrold Olefsky; Warren Tourtellotte; John Varga Journal: Arthritis Res Ther Date: 2018-07-11 Impact factor: 5.156