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. 2020 Dec 1;9:20. doi: 10.1186/s13619-020-00058-0

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© The Author(s) 2020

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 1 — Pathophysiology of Systemic Sclerosis (SSc). In the pathophysiology of SSc first of all, an immune dysregulation is caused that is displayed by auto antibody production. The mechanism during which the dyscrasias is caused, is not completely understood, but it is proposed that genetics and the environmental factors play important roles in the process. Autoantibodies as well as other factors like high levels of reactive oxygen species(ROS) cause vascular injury, the process that leads to the activation of fibroblasts. Activated fibroblasts produce an unusual high amount of collagen (especially type I) as well as other components of extracellular matrix (ECM) that form an extensive amount of fibrosis (Velier et al. 2019)