Key result
Multi-omic profiling identifies 4 cerebral atherosclerosis phenotypes and 6 overexpressed genes in severe stenosis.
Why the study?
Cerebral atherosclerosis shows marked clinical and molecular heterogeneity, and conventional laboratory parameters do not always adequately reflect atherosclerotic burden and disease activity, creating a need to define phenotypes using novel epigenetic and molecular-genetic markers.
Observational (n=80)
Integrated analysis of microRNAs, cardiovascular panel genes, and clinical data identifies four distinct phenotypes of cerebral atherosclerosis, offering a potential molecular basis for personalized risk stratification and management in cerebrovascular disease.
Answers are grounded in this paper and cite their sources.
May refine cerebral atherosclerosis phenotyping via microRNA expression; hypothesis-generating and requires prospective validation.
Background. Cerebral atherosclerosis is one of the leading causes of ischemic stroke and shows marked clinical and molecular heterogeneity. Conventional laboratory parameters do not always adequately reflect atherosclerotic burden and disease activity, highlighting the need for novel epigenetic and molecular-genetic markers of atherogenesis. Aim: to identify clinical and molecular phenotypes of cerebral atherosclerosis based on the integrated analysis of clinical data and the expression of microRNAs and atherosclerosis-associated genes. Material and methods. Eighty patients with cerebral atherosclerosis (median age 66 years) were enrolled in this prospective study. Leukocyte expression of 8 microRNAs (miR-126, miR-29, miR-33a, miR-21 families) was assessed by Real-time PCR, and 54 cardiovascular panel genes were profiled with the nanoString nCounter platform. Differential expression, correlation (Spearman with FDR correction), cluster (FAMD/HCPC), and co-expression network analyses were performed. Results. Differential expression of miR-126-3p/-5p, miR-29-3p, miR-33a-5p/-3p, and miR-21-3p was demonstrated according to the severity of carotid stenosis, alongside overexpression of 6 genes (ABCA7, MTHFR, TNF, PLEKHG1, SORL1, CCDC127) in patients with ICA stenosis ≥ 70%. Significant inverse correlations between miR-126 and proatherogenic genes were established. Cluster analysis identifi ed 4 clinical and molecular phenotypes — “endothelioprotective/early”, “moderate/reference”, “systemic atherosclerotic”, and “cerebrometabolic” — refl ecting the continuum of disease progression. Conclusion. The study confirmed the clinical and molecular heterogeneity of cerebral atherosclerosis with the identifi cation of four distinct phenotypes reflecting different trajectories of disease progression. These findings may serve as a basis for personalized approaches to risk stratification, diagnosis, and treatment of patients with cerebrovascular disease.
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Раскуражев et al. (2026) conducted an observational in Cerebral atherosclerosis (n=80). Leukocyte expression of 8 microRNAs and 54 cardiovascular panel genes vs. Varying severity of carotid stenosis (including ICA stenosis ≥70%) was evaluated on Clinical and molecular phenotypes of cerebral atherosclerosis based on clinical data, microRNA expression, and atherosclerosis-associated gene expression. Integrated clinical, microRNA, and gene expression profiling in 80 cerebral atherosclerosis patients identified 4 distinct phenotypes and 6 overexpressed genes in ICA stenosis ≥70%.
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