Objectives: Emerging evidence shows that
integrin members are involved in
inflammation and
fibrosis in
systemic sclerosis (SSc). This study aimed at evaluating the expression of
integrin family genes in the skin tissue from SSc patients and exploring the potential pathogenic mechanism. Methods: We utilized the public datasets of SSc skin tissue from the Gene Expression Omnibus (GEO) database to analyze the expression and clinical significance of
integrin family genes in SSc. The expression of
integrin members in skin tissue was also assessed by immunohistochemistry. In addition, functional enrichment and pathway analysis were conducted. Results: Compared with healthy controls, the
mRNA and
protein levels of ITGA5, ITGB2, and ITGB5 were upregulated in the skin of SSc patients. Further analysis indicated that the
mRNA expression levels of ITGA5, ITGB2, and ITGB5 were positively correlated with modified Rodnan skin thickness score (mRSS). Functional enrichment and pathway analysis showed that
integrin members may play multiple roles in the pathogenesis of SSc. Among them, ITGA5, ITGB2, and ITGB5 might synergistically promote SSc through affecting extracellular matrix (ECM) turnover, ECM-receptor interaction, focal adhesion, and leukocyte trans-endothelial migration, while ITGA5 and ITGB5 also might affect angiogenesis and endothelial cell function. In addition, ITGA5, ITGB2, and ITGA5 were associated with different pathways, respectively. ITGA5 was uniquely enriched for actin organization, while ITGB5 was for TGF-β signaling and ITGB2 for immune cell activation. Conclusion: Our results implied that the abnormal expression of
integrin family genes including ITGA5, ITGB2, and ITGB5 may participate in multiple
pathological processes in SSc. Further investigations are required for confirming this speculation.