Oxidized LDL and macrophage activation in atherosclerosis: Molecular mechanisms, immunological plasticity, and novel therapeutic strategies
Keywords:
atherosclerosis, oxLDL, macrophage polarizationAbstract
This analytical article is devoted to studying the central link in the pathogenesis of atherosclerosis — the molecular interaction between oxidized low-density lipoproteins (oxLDL) and macrophages. Atherosclerosis is not just a buildup of cholesterol, but a complex chronic immune-inflammatory process in the arterial wall. The paper analyzes the absorption of oxldl by scavenger-receptors (CD36, PAFR, LOX-1), polarization of macrophages to phenotypes M1 (pro-inflammatory) and M2 (anti-inflammatory), and signaling pathways (TLR4/NF-kB, eEF2K) that control these processes. The analysis provides scientific evidence for recent scientific discoveries over the past 10 years, particularly the mechanisms by which macrophages survive in stressful conditions and the anti-atherosclerotic effects of natural compounds such as Puerarin.The findings of the study will help identify new molecular targets for atherosclerosis therapy
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