Behavior of Complement System Effectors in Chronic and Acute Coronary Artery Disease

Figures

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  Figure 1. Boxplot of sC5b-9 value distributions for the three categories of patients (left). Outliers are marked with a circle. The statistically significant differences between groups were confirmed by the Kruskal–Wallis test (right).

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  Figure 2. Predictive ability of sC5b-9 to differentiate patients with NSTEMIs from the control group. ROC curves: The blue curve depicts the performance of sC5b-9 as a biomarker, while the red diagonal line represents random classification. The area under the curve (AUC) is 0.702, indicating a moderate discriminative ability of sC5b-9 in distinguishing NSTEMI patients from controls.

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  Figure 3. RGC-32 value distributions for the three categories of patients (left). Outliers in the boxplot are marked with a circle, and extreme outliers with an asterisk. The statistically significant difference between groups was confirmed by a Kruskal–Wallis test (right).

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  Figure 4. Correlation between RGC-32 and sC5b-9 in patients with APS.

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  Figure 5. RGC-32 levels in patients with and without myocardial infarction among those with APS. The statistically significant difference was confirmed by the Mann–Whitney test.

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  Figure 6. Boxplot of SIRT1 value distributions for the three categories of patients. The statistically significant difference between groups was confirmed by a Kruskal–Wallis test. Outliers are marked with a circle, and extreme outliers with an asterisk.

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  Figure 7. Hypothetical model of the dual role of RGC-32 in the different stages of CAD (adapted from [21]; created in https://BioRender.com). (A) In atherosclerotic plaques from stable, chronic, ischemic CAD, RGC-32 plays a pro-atherogenic role; in endothelial cells, RGC-32 mediates complement C5b-9-induced cell cycle activation and migration; similarly, in smooth muscle cells, RGC-32 participates in the C5b-9-induced proliferation of SMCs and TGF-β-dependent phenotype modulation in SMCs, which can favor extracellular matrix ECM deposition and a synthetic phenotype. (B) In cardiomyocytes from patients with a prior MI (ischemia-damaged myocardium), the expression of RGC-32, induced by either complement C5b-9 or by TGF-β, could have an antifibrotic, protective effect against cardiac fibrosis.