Clinical Study on NAFLD Intervening in the Progression of Coronary Atherosclerosis by Affecting TREM2-Related Inflammatory Pathways Regulated by Adipose Tissue

Abstract Objective : To investigate the effect of non-alcoholic fatty liver disease (NAFLD) on the progression of coronary atherosclerotic heart disease (CCS) and its association with TREM2-related inflammatory pathways.

Methods: A total of 56 CCS inpatients were divided into the NAFLD+CCS group (n=33) and CCS group (n=23) based on NAFLD diagnostic criteria. Basic clinical and biochemical indicators, liver/visceral fat content, and coronary atherosclerosis severity (GS score) were detected. Monocyte subsets (classical CD14++CD16-, intermediate CD14++CD16+, non-classical CD14+CD16++) were analyzed by flow cytometry. Serum sTREM2, IL-6, and IL-10 concentrations were measured by ELISA or enzyme-linked immunosorbent assay. Results Compared with the CCS group, the NAFLD+CCS group had significantly higher absolute monocyte count (MO), hs-CRP, GS score, and sTREM2 concentration (all P<0.05). Regarding monocyte subsets, the proportion of classical monocytes (CM) was lower (80.12%±4.38% vs. 83.93%±5.35%, P=0.005), while intermediate (IM: 4.83%±1.48% vs. 3.25%±1.53%, P=0.000) and non-classical monocytes (NCM: 8.53%±3.26% vs. 6.50%±3.17%, P=0.024) were higher in the NAFLD+CCS group. Levels of IL-6 and IL-10 were also significantly elevated in the NAFLD+CCS group (both P<0.001). Conclusion : NAFLD exacerbates systemic inflammation and coronary atherosclerosis in CCS patients, accompanied by abnormal monocyte subset distribution and increased sTREM2. It is speculated that TREM2 may regulate macrophage polarization via the PI3K/AKT/NF-κB pathway, thereby mediating adipose tissue inflammation and participating in NAFLD-related atherosclerosis progression.