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The latter is triggered by mediators released from activated leukocytes, such as tumor necrosis factor (TNF), interleukin 1 beta (IL-1) and 6 (IL-6), which induce endothelial cell acquisition of a pro-inflammatory transcriptional program (6, 7)

Overexpression of PHB2 can activate mitophagy, restore mitochondrial activity, enhance myocardial cell viability, and inhibit endotoxin-induced mitochondrial dysfunction in myocardial cells [15]