Abstract
Systemic sclerosis (SSc) is an autoimmune disease with fibrosis of the skin and/or internal organs, causing a decrease in quality of life and survival. There is no causative therapy, and the pathophysiology of the SSc remains unclear. Studies showed that lipid metabolism was relevant for autoimmune diseases, but little is known about the role of lipids in SSc. In the present study, we sought to explore the phospholipid profile of SSc by using the lipidomics approach. We also aimed to analyze lipidomics results for different clinical manifestations of SSc. Experiments were performed using high-performance liquid chromatography coupled to mass spectrometry for the lipidomic profiling of plasma samples from patients with SSc. Our study showed, for the first time, significant changes in the level of phospholipids such as plasmalogens and sphingomyelins from the plasma of SSc patients as compared to controls. Phosphatidylcholine plasmalogens species and sphingomyelins were significantly increased in SSc patients as compared to controls. Our results also demonstrated a significant association of changes in the metabolism of phospholipids (phosphatidylcholine and phosphatidylethanolamine plasmalogens species and sphingomyelins) with different clinical manifestations of SSc. Further lipidomic studies might lead to the detection of lipids as new biomarkers or therapeutic targets of SSc.
Highlights
Systemic sclerosis (SSc) is a chronic autoimmune disease that leads to fibrosis of the skin and/or internal organs and endothelial damage [1]
Management of SSc has improved during the last years [3,4], there is no causative treatment for SSc, and the pathophysiology is still unclear
SSc patients had a mean age of 60 years, and 44 patients were female
Summary
Systemic sclerosis (SSc) is a chronic autoimmune disease that leads to fibrosis of the skin and/or internal organs and endothelial damage [1]. The most frequent cause of death in SSc patients is progressive lung fibrosis (LF). The quality of life in SSc patients is decreased due to multi-organ manifestations of SSc, such as thickening of the skin, chronic digital ulcers (DU), pain and superinfections due to calcinosis cutis (CC), dyspnea due to lung disease or dry mouth, and eyes due to sicca mucositis [2]. Clinical manifestations and autoantibody profiles are often specific for these two subsets of SSc. Anti-centromere antibodies (ACA) are frequently associated with lcSSc and anti-Scl70-antibodies (anti-topoisomerase I-antibodies) with dcSSc. management of SSc has improved during the last years [3,4], there is no causative treatment for SSc, and the pathophysiology is still unclear
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