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Alterations of Extracellular Matrix Components in the Course of Juvenile Idiopathic Arthritis
Magdalena Wojdas1, Klaudia Dąbkowska1, Katarzyna Winsz-Szczotka1
1Department of Clinical Chemistry and Laboratory Diagnostics, Faculty of Pharmaceutical Sciences in Sosnowiec, Medical University of Silesia, ul. Jedności 8, 41-200 Sosnowiec, Poland.
Insights
Juvenile idiopathic arthritis (JIA) involves joint damage due to inflammation and altered extracellular matrix (ECM) metabolism. Reviewing catabolic factors in children with JIA may reveal new diagnostic and therapeutic strategies.
Area of Science:
- Rheumatology
- Pediatric Medicine
- Biochemistry
Background:
- Juvenile idiopathic arthritis (JIA) is a prevalent chronic childhood connective tissue disease.
- Inflammation and proinflammatory cytokines drive articular cartilage destruction in JIA.
- Disrupted extracellular matrix (ECM) homeostasis underlies progressive joint damage.
Purpose of the Study:
- To review enzymatic and non-enzymatic factors in ECM component catabolism.
- To examine molecules that stimulate ECM component biosynthesis.
- To discuss the diagnostic potential of these factors in JIA disease activity assessment.
Main Methods:
- Literature review of enzymatic and non-enzymatic factors.
- Analysis of ECM component metabolism in JIA.
- Evaluation of potential biomarkers in body fluids.
Main Results:
- JIA involves dysregulated ECM metabolism, impacting proteoglycans and cartilage.
- Specific catabolic factors and biosynthesis regulators are altered in JIA.
- Changes in these factors in body fluids show potential for disease assessment.
Conclusions:
- Understanding ECM changes in JIA is crucial for developing new diagnostic tools.
- Identifying key factors in ECM metabolism may lead to novel therapeutic strategies for JIA.
- Biomarkers related to ECM turnover could improve JIA management.
Abstract:
Juvenile idiopathic arthritis (JIA) is the most common group of chronic connective tissue diseases in children that is accompanied by joint structure and function disorders. Inflammation underlying the pathogenic changes in JIA, caused by hypersecretion of proinflammatory cytokines, leads to the destruction of articular cartilage. The degradation which progresses with the duration of JIA is not compensated by the extent of repair processes. These disorders are attributed in particular to changes in homeostasis of extracellular matrix (ECM) components, including proteoglycans, that forms articular cartilage. Changes in metabolism of matrix components, associated with the disturbance of their degradation and biosynthesis processes, are the basis of the progressive wear of joint structures observed in the course of JIA. Clinical evaluation and radiographic imaging are current methods to identify the destruction. The aim of this paper is to review enzymatic and non-enzymatic factors involved in catabolism of matrix components and molecules stimulating their biosynthesis. Therefore, we discuss the changes in these factors in body fluids of children with JIA and their potential diagnostic use in the assessment of disease activity. Understanding the changes in ECM components in the course of the child-hood arthritis may provide the introduction of both new diagnostic tools and new therapeutic strategies in children with JIA.
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