ArticleBMC neurology2026
Effect of the atherogenic index of plasma on the expression of platelet CD36 and CD62P in patients with acute ischemic stroke: a retrospective study from Tianjin, China.
Article in BMC neurology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectiveThe atherogenic Index of Plasma (AIP) is closely linked to the incidence of acute ischemic stroke (AIS). This study aimed to investigate the effect of AIP on the expression levels of platelet surface markers CD36 and CD62P in AIS patients, and further analyze the correlations among these three indicators.
methodsThis retrospective study enrolled 441 AIS patients who underwent platelet flow cytometry and were admitted between January 2024 and June 2025. Participants were stratified by AIP tertiles. Platelet CD36 and CD62P expression levels were detected via flow cytometry. Multivariate adjusted regression models and linear regression analyses were performed to explore the relationships between AIP and platelet CD36/CD62P expression. Stratified analyses were conducted by potential risk factors to examine subgroup differences. A generalized additive model (GAM) with smooth curve fitting was used to investigate the association pattern between CD36 and CD62P. Simple mediation analysis via the bootstrap method was applied to explore the potential mediating effect of CD36 in the relationship between AIP and CD62P.
resultsAIP, whether considered as a continuous or a categorical variable, was significantly correlated with platelet CD62P levels. For each 1-unit increase in AIP, CD62P levels rose by 1.62 (β = 1.62, 95% CI: 0.41–2.82, P = 0.009). When AIP was divided into tertiles, the highest tertile (Q3) showed a significant increase in CD62P levels compared to the lowest (Q1), with a significant dose-response trend (P < 0.05). AIP also showed a significant positive correlation with CD36 (β = 2.30, 95% CI: 0.43–4.16, P = 0.016), with significant differences in CD36 levels in both middle (Q2) and highest tertiles (Q3) compared to Q1. The GAM with smooth curve fitting showed that higher CD36 expression led to increased platelet CD62P levels (95% CI:11.19–12.87), confirming a significant nonlinear relationship (P = 0.0017). A mediation model indicated that CD36 partially mediates the effect of AIP on CD62P.
conclusionIn AIS patients, high AIP levels are linked to increased platelet markers CD36 and CD62P, as well as dyslipidemia and atherosclerosis. AIP has the potential to serve as a significant biomarker for assessing platelet activity.
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