In the Pursuit of Metabolic Markers of Systemic Sclerosis-Plasma Adiponectin and Omentin-1 in Monitoring the Course of the Disease

Systemic sclerosis (SSc) is a connective tissue disease leading to cutaneous and visceral fibrosis. Pathological features of SSc include immune dysregulation, vasculopathy, and impaired angiogenesis. Adipokines act as cytokines and hormones and are involved in various pathological processes, includi...

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Published in:International journal of molecular sciences Vol. 24; no. 12; p. 9988
Main Authors: Dopytalska, Klaudia, Kalisz, Małgorzata, Litwiniuk, Anna, Walecka, Irena, Bik, Wojciech, Baranowska-Bik, Agnieszka
Format: Journal Article
Language:English
Published: Switzerland MDPI AG 01-06-2023
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Summary:Systemic sclerosis (SSc) is a connective tissue disease leading to cutaneous and visceral fibrosis. Pathological features of SSc include immune dysregulation, vasculopathy, and impaired angiogenesis. Adipokines act as cytokines and hormones and are involved in various pathological processes, including metabolic disorders, inflammation, vasculopathy, and fibrosis. This study aimed to determine the level of omentin-1 and adiponectin to evaluate their potential role in the pathogenesis of SSc. We assessed serum omentin-1 and adiponectin as well as metabolic parameters in 58 patients with SSc and 30 healthy controls. The follow-up was performed in SSc individuals. Omentin-1 levels were significantly higher in SSc individuals as compared to the controls. In post-hoc analysis, omentin-1 was higher in the group with disease duration ≥7 years than in the control group. A positive correlation was noted between disease duration and both adipokines and increased with longer disease duration. However, there were no correlations between selected adipokines and metabolic parameters. Enhanced omentin-1 levels and higher levels of omentin-1 in patients with longer disease duration may suggest that omentin-1 is involved in the pathomechanisms of SSc as its concentrations are not directly related to BMI, age, and insulin resistance.
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ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms24129988