Background
Systemic lupus erythematosus is a chronic multisystemic autoimmune disease characterized by chronic inflammatory processes and failure of immune-regulatory mechanisms. Systemic lupus erythematosus is associated with increased risk for cardiovascular disease. In view of immunometabolic derangements of systemic lupus erythematosus, we investigated the roles of sucrose non-fermenting AMPK related kinase, Pentraxin 3, and DNA damage in the pathogenesis of systemic lupus erythematosus complicated with cardiovascular disease.
Conclusions
These data highlight a novel role of sucrose non-fermenting AMPK related kinase/Pentraxin 3 axis in systemic lupus erythematosus pathogenesis. Sucrose non-fermenting AMPK related kinase/Pentraxin 3 combined role in immunometabolic signaling and DNA damage response is proposed to accelerate cardiovascular complications in systemic lupus erythematosus patients.
Methods
Forty systemic lupus erythematosus women with cardiovascular disease (systemic lupus erythematosus cases), 40 systemic lupus erythematosus women without cardiovascular disease, and 40 healthy controls were enrolled in this study. Demographic and clinical data were recorded. Plasma concentrations of sucrose non-fermenting AMPK related kinase and Pentraxin 3 were immunoassayed. Carotid intima media thickness, atherogenic, and DNA damage indices were also assessed.
Results
Plasma sucrose non-fermenting AMPK related kinase and Pentraxin 3 concentrations were increased in systemic lupus erythematosus cases with cardiovascular disease compared to systemic lupus erythematosus controls and healthy controls (P < 0.0001). In systemic lupus erythematosus cases, there was a positive correlation between sucrose non-fermenting AMPK related kinase and Pentraxin 3 (r = 0.57, P < 0.002). Conclusions: These data highlight a novel role of sucrose non-fermenting AMPK related kinase/Pentraxin 3 axis in systemic lupus erythematosus pathogenesis. Sucrose non-fermenting AMPK related kinase/Pentraxin 3 combined role in immunometabolic signaling and DNA damage response is proposed to accelerate cardiovascular complications in systemic lupus erythematosus patients.