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Heinemann et al., 1959

TB-500's Ac-SDKP fragment inhibits macrophage migration inhibitory factor (MIF) in cell culture models

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(36) demonstrated that key signaling pathwaysincluding the Nrf2-Keap1 pathway, p53, and Hippo pathwaycontribute to the initiation and progression of atherosclerosis by modulating the expression and activity of ferroptosis-related proteins

The proposed mechanism is two-fold: transplanted mitochondria can directly supply ATP to energy-starved cells and can also modulate immune cells by reducing DAMPs release and apoptosis