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Following stimulation by various physiological factors (such as inflammatory triggers, vascular damage, and hemodynamic perturbations), contractile VSMCs in the normal aortic wall lose their unique structure and function, and undergo phenotypic switching to synthetic VSMCs, which is characterized by enhanced abilities of proliferation and migration, and increased secretion of various extracellular matrix proteins and cytokines (77)
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Also, the MWM is not conducive to certain mouse strains [90, 189]
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