Cyclophilin A and matrix metalloproteinase-9: Their relationship, association with, and diagnostic relevance in stable coronary artery disease

Objectives Data about the circulating levels of cyclophilin A and matrix metalloproteinase-9 in stable coronary artery disease are contradictory. Moreover, their relationship in this disease is not established yet. Thus, this study was designed to assess the relationship between the circulating levels of cyclophilin A and matrix metalloproteinase-9 in coronary artery disease patients with and without type 2 diabetes mellitus (T2DM). Methods Serum levels of cyclophilin A, matrix metalloproteinase-9, and high sensitive C-reactive protein (hsCRP) along with fasting blood glucose, glycated hemoglobin, serum lipids, and the anthropometric parameters were measured in 120 participants who were divided equally into four groups (i) normal controls, (ii) T2DM patients, (iii) stable coronary artery disease patients with T2DM, and (iv) stable coronary artery disease patients without T2DM. Results Levels of cyclophilin A and matrix metalloproteinase-9 were significantly elevated in sera of coronary artery disease patients with and without T2DM compared to normal controls and T2DM patients. In multiple linear regression models, only cyclophilin A was observed in the final model where it explained the 24.9% variability of matrix metalloproteinase-9. Additionally, high circulating levels of cyclophilin A and matrix metalloproteinase-9 were associated with an increased risk of developing stable coronary artery disease. Finally, the diagnostic efficacy of cyclophilin A and matrix metalloproteinase-9 to discriminate stable coronary artery disease patients with and without T2DM from subjects without coronary artery disease was found to be higher than that of hsCRP. Conclusion Serum level of cyclophilin A might be a determinant factor of matrix metalloproteinase-9 level; both may contribute to the pathogenesis of stable coronary artery disease and they appear to be valuable diagnostic biomarkers of stable coronary artery disease with and without T2DM.