Key result
Atherosclerosis displays bed-specific inflammatory mechanisms across arterial territories, arguing for tailored therapies.
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This review highlights the distinct immune-inflammatory pathways driving atherosclerosis in different vascular beds, emphasizing the potential need for bed-specific and patient-specific treatment strategies.
Studies suggest varying atherosclerotic cardiovascular disease (ASCVD) prevalence across arterial beds. Factors such as smoking expedite ASCVD progression in the abdominal aorta, while diabetes accelerates plaque development in lower limb arteries, and hypertension plays a significant role in ASCVD development in the coronary and carotid arteries. Moreover, superficial femoral atherosclerosis advances slower compared with atherosclerosis in coronary and carotid arteries. Furthermore, femoral atherosclerosis exhibits higher levels of ossification and calcification, but lower cholesterol concentrations compared with atherosclerotic lesions of other vascular beds. Such disparities exemplify the diverse progression of ASCVD across arterial beds, pointing towards differential mechanistic pathways in each vascular bed. Hence, this review summarizes current literature on immune-inflammatory mechanisms in various arterial beds in ASCVD to advance our understanding of this disease in an aging society with increased need of vascular bed and patient-specific treatment options.
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Soehnlein et al. (2025) conducted a review in Atherosclerotic cardiovascular disease (ASCVD). Immune-inflammatory mechanisms in various arterial beds was evaluated. Atherosclerotic cardiovascular disease exhibits diverse progression and distinct immune-inflammatory mechanisms across different arterial beds, necessitating patient-specific treatment options.
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