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It was estimated that the population with diabeties worldwide would increase from 451 million people in 2017 to 693 million by 2045 2

The underlying mechanism for hyperhomocysteinemia-induced NLRP3 inflammasome activation is through the generation of ROS (Wang et al

IV therapy typically refers to short-term hydration, vitamin-nutrient enhancements, or wellness-focused treatments

SCFAs activate GPCR41/43 to reduce hepatic cholesterol synthesis, inhibit NF-B-mediated inflammation, and enhance endothelial nitric oxide (NO) production ( / mice, SCFAs reduce aortic plaque area by 3040% ( 3.2 Inflammatory activation: LPS and cytokine cascades Gut barrier disruption (reduced occludin, ZO-1 expression) allows LPS translocation, activating TLR4/NF-B signaling in macrophages and endothelial cells ( 3.3 Vascular dysfunction: endothelial injury and oxidative stress Dysbiosis-derived metabolites (TMAO, LPS) and reduced SCFAs impair endothelial function by decreasing NO bioavailability and increasing reactive oxygen species (ROS) ( 4 Probiotics in atherosclerosis: mechanisms of action Probiotics exert anti-atherosclerotic effects through strain-specific modulation of gut microbiota, metabolic homeostasis, inflammation, and vascular function ( Table 1 )