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doi: 10.1186/s13024-020-00368-6 18 AlamMMYangDLiX-QLiuJBackTCTrivettAet al
doi: 10.1186/S13023-021-01781-W
The secondary lesions of AS include lipid deposition, intimal thickening, thrombosis, inflammatory cell infiltration, subintimal inflammation, vessel wall remodeling, neovascularization, plaque rupture, intraplaque hemorrhage, plaque rupture and local thrombosis, which eventually cause narrowing or blockage of the vascular lesion, resulting in ischemic injury to the affected organs (4)
doi: 10.1212/WNL.30.7.772
J Biol Chem 2013;288:3607382
