The influence of endothelial microparticles on carotid atherosclerosis in geriatric schizophrenia: the mediating role of inflammatory cytokines and the moderating role of metabolic syndrome.

OBJECTIVE

The present study aimed to investigate the relationship between endothelial microparticles (EMPs) and carotid atherosclerosis in geriatric patients with schizophrenia (SCH), as well as whether metabolic syndrome (MS) and immune-inflammatory markers play a mediating or moderating role on this pathway.

METHODS

A total of 92 geriatric patients with SCH and 63 healthy controls (HC) were included in this study. Plasma levels of endothelial microparticles and inflammatory cytokines (interleukin (IL)-2, IL-4, IL-6, IL-10, tumor necrosis factor (TNF)-α, granulocyte-macrophage colony-stimulating factor (GM-CSF), IL-1β, interferon (IFN)-γ), blood glucose and lipid components, and carotid intima-media thickness (CIMT) were measured in all participants. Based on the diagnostic criteria for MS in the Chinese Type 2 Diabetes Prevention and Treatment Guidelines (2020 edition), participants were divided into MS and non-MS (NMS) groups.

RESULTS

We found that geriatric SCH patients had significantly lower IL-4 levels (p < 0.001) and higher levels of IL-6, TNF, IL-1β, EMPs and CIMT (all p < 0.001) compared to the matched HC. Moreover, our results showed that geriatric SCH patients with MS had markedly higher IL-1β, CIMT and EMPs levels, but lower IL-4 than SCH-NMS group. Pearson correlation analysis showed that circulating EMPs counts, IL-6 and GM-CSF were positively, whereas IL-4 was negatively, correlated with CIMT in geriatric SCH. Moderated mediation analyses revealed that IL-4 and IL-6 mediated the relationship between EMPs and CIMT, and MS moderated this mediation model.

CONCLUSION

Our study suggests that EMPs may be associated with carotid atherosclerosis in geriatric SCH, in which immune-inflammatory factors (IL-4 and IL-6) may play a mediating role and MS may act as a moderator in this pathway. These findings may provide preliminary insights into the potential pathogenesis of atherosclerosis-related cardiovascular diseases in geriatric patients with SCH.