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Ultra-processed foods (UPFs) now dominate dietary intake in many countries and are consistently associated with higher risks of cardiovascular disease (CVD), including myocardial infarction, stroke, and heart failure. Beyond excess sodium, sugar, and unhealthy fats, UPFs may exert cardiovascular harm through food matrix disruption, processing-generated toxicants, additive exposure, and microbiome perturbation. These upstream insults converge on inflammatory, oxidative, and metabolic signaling pathways that regulate microRNAs (miRNAs), a class of small non-coding RNAs that orchestrate post-transcriptional gene expression across endothelial cells, vascular smooth muscle cells, macrophages, platelets, and metabolic tissues. In this review, we propose a unifying mechanistic framework in which UPF exposure reshapes both intracellular and extracellular vesicle (EV)-associated miRNA networks, thereby linking gut, liver, adipose tissue, and the vascular wall in a feed-forward cardiometabolic signaling loop. We synthesize evidence across epidemiology, experimental models, and human dietary intervention studies, while explicitly distinguishing established, emerging, and speculative mechanisms to avoid over-interpretation. We further discuss translational opportunities, including circulating miRNA/EV-miRNA biomarkers, nutritionally responsive miRNA signatures, and miRNA-targeted therapeutics. Together, this framework positions the UPF-miRNA/EV axis as a plausible molecular bridge between modern dietary exposure and atherosclerotic disease progression, and highlights priority areas for mechanistic validation and clinical translation.
Wen et al. (Mon,) studied this question.