Abnormal oxidative stress has been found in SSc patients, that is, excessive production of ROS and an imbalance between oxidation and oxidation, and its effect with the inflammatory response (i.e., the effect of ROS on macrophage polarization and activation of inflammasome NLRP3 (78)) may promote the development of vascular lesions, and its induction effect on autoimmune disorders, endothelial dysfunction, and fibrosis is conducive to maintaining the pro-inflammatory state of SSc (79, 80). This evidence concerns the gene NLRP3 and systemic sclerosis.