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Dyslipidemia, particularly the elevation of lowdensity lipoprotein cholesterol (LDL-C) levels, is the prerequisite for the occurrence and development of plaque-based atherosclerotic cardiovascular disease (ASCVD). LDL particles pass through the vascular endothelium and become lodged within the walls of blood vessels. Oxidative modification of LDL then occurs under the action of extracellular matrix molecules, followed by foam cell formation after macrophage phagocytosis. Subsequently, there occur localized biological responses, mainly non-specific inflammation, which further promotes LDL retention and atherosclerotic lesion progression. A large number of clinical studies has repeatedly confirmed that, regardless of the medication type or intervention method, as long as the plasma LDL-C level is reduced, atherosclerotic lesions can be stabilized, impeded, or alleviated. TheASCVD incidence aswell as morbidity and mortality rates will also decrease significantly. Domestic and international dyslipidemia prevention guidelines have all emphasized that LDL-C plays a central and pathogenic role in ASCVD. Hence, the prevention and control of ASCVD risk by decreasing

chronic diseases and translational medicine

Amendment of the low‐density lipoprotein cholesterol target in the ‘Chinese Guidelines for the Prevention and Treatment of Adult Dyslipidemia’: Opinion