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. 2019 May 16;7(5):e2228. doi: 10.1097/GOX.0000000000002228

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Copyright © 2019 The Authors. Published by Wolters Kluwer Health, Inc. on behalf of The American Society of Plastic Surgeons.

This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal.

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Fig. 2. — A proposed model of keloid disorder demonstrating the potential source of dysregulated fibroblasts and myofibroblasts, characteristic of keloid lesions. Following an injury, the embryonic stem cells (ESC)-like cells on the endothelium of the microvessels give rise to mesenchymal stem cells (MSCs) through a process of endothelial-to-mesenchymal transition (Endo-MT) induced by cytokines such as transforming growth factor-β1 (TGF-β1). These MSCs undergo differentiation into aberrant fibroblasts and myofibroblasts, characteristic excessive extracellular matrix deposition, and fibrosis seen in keloid lesions. This process is regulated by the renin-angiotensin system (RAS) and the immune system/inflammatory process. Through Endo-MT, these aberrant fibroblasts and myofibroblasts may also be derived from circulating MSCs and fibrocytes from the bone marrow which migrate to the target tissues.