Related Experiment Video
Updated: May 9, 2026
04:44
Imaging Features of Systemic Sclerosis-Associated Interstitial Lung Disease
Published on: June 16, 2020
Serum galectin-3 level in systemic sclerosis.
Suleyman Serdar Koca1, Fatma Akbas, Metin Ozgen
1Department of Rheumatology, Faculty of Medicine, Firat University, 23119, Elazig, Turkey, kocassk@yahoo.com.
Clinical Rheumatology
|August 6, 2013
Summary
Serum galectin-3 levels are elevated in patients with Systemic Sclerosis (SSc) and Systemic Lupus Erythematosus (SLE). Higher galectin-3 indicates active disease, suggesting its potential as a biomarker for SSc activity.
Area of Science:
- Immunology
- Rheumatology
- Biochemistry
Background:
- Systemic sclerosis (SSc) is an autoimmune disease causing progressive fibrosis, primarily driven by activated fibroblasts.
- Galectin-3, a β-galactoside-binding lectin, is implicated in regulating cellular processes like proliferation, apoptosis, inflammation, and fibrosis.
Purpose of the Study:
- To investigate and assess serum galectin-3 levels in patients diagnosed with Systemic Sclerosis (SSc).
Main Methods:
- Serum galectin-3 levels were measured in 37 SSc patients, 23 Systemic Lupus Erythematosus (SLE) patients, and 28 healthy controls.
- Disease activity and severity were assessed using established indices (Valentini, Medsger, SLEDAI, SLICC/ACR).
- Levels of vascular endothelial growth factor, transforming growth factor-β, and interleukin-6 were also determined.
Main Results:
- Serum galectin-3 levels were significantly higher in both SSc and SLE patient groups compared to healthy controls.
- While not correlated with overall disease severity scores, galectin-3 levels were notably higher in active SSc and active SLE subgroups versus their inactive counterparts.
- Specific p-values: SSc (p=0.015), SLE (p=0.019) for active vs. inactive subgroups.
Conclusions:
- Elevated serum galectin-3 may serve as a potential biomarker for disease activity in Systemic Sclerosis.
- Galectin-3's association with fibrosis and inflammation supports its role in SSc pathogenesis.
