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TBP-2 amplifies inflammatory response, apoptosis, and the reduction of stress fiber formation. Under oxidative stress, overexpressed TBP-2 results in the activation of the NLRP3 inflammasome, IL-1β and cell apoptosis and, ultimately, cardiomyopathy. Under a disturbed flow, overexpressed TBP-2 regulates a SHP2-CSK-Src signaling cascade, so that the cardiovascular system is susceptible to atherosclerosis.
