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Inflammation is a key component and contributor in the pathophysiology of ischemia, existing in every stage of the ischemic cascade (Iadecola and Anrather, 2011)

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Recent studies demonstrated that Notch signaling is required for the adhesion of VSMCs but not other types of VSMC-derived cells in the formation of the cap in mouse atherosclerosis, and reduction of Notch signaling is a prerequisite for medial VSMC mediating the development of plaque, 248 suggesting that sequential loss and gain of Notch signaling is required for the recruitment of cap SMC population in atherosclerosis