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Findings indicate dysregulated lipid metabolism relates to atherosclerotic plaque burden in individuals with type 2 diabetes.
Atherosclerotic cardiovascular disease (ASCVD) remains a leading cause of death despite recent therapeutic advances. Infiltration and oxidative modification of low-density lipoprotein (LDL) cholesterol in the arterial wall and chronic inflammation comprise central pathogenetic mechanisms in ASCVD. Scavenger receptors, particularly Stabilin-1 (STAB1) and Stabilin-2 (STAB2), are pivotal in the clearance of oxidized LDL (oxLDL) cholesterol and pro-atherogenic ligands from circulation. However, their role in atherosclerosis development remains poorly characterized. We assessed circulating levels of STAB1, STAB2 and their ligands (TGFBI, Periostin and Reelin) in a cohort of 54 individuals, stratified by their atherosclerotic plaque burden as assessed by high-resolution vascular ultrasound. A subgroup analysis of 33 individuals with type 2 diabetes mellitus, a leading cause of ASCVD, was also performed. Associations between stabilins, their ligands and conventional cardiovascular risk factors were evaluated. STAB1 levels were significantly elevated in individuals with higher atherosclerotic plaque burden (p<0.05), while Reelin levels were marginally elevated, both in the total study cohort and among T2DM individuals. STAB1 levels positively correlated with body mass index and inversely correlated with total cholesterol, LDL and high-density lipoprotein (HDL) cholesterol levels. These findings indicate that STAB1 may serve as a marker of dysregulated lipid metabolism and increased atherosclerotic plaque burden in the general population, as well as in individuals with T2DM. Larger prospective studies are warranted to establish the prognostic and potentially therapeutic value of STAB1 and to clarify its mechanistic role in diabetic atherosclerosis.
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Giannousi et al. (2025) studied this question.
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