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To date, no study has targeted the ferroptosis pathway in thyroid cancer as a therapeutic option
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Monomeric C-reactive protein affects cell injury and apoptosis through activation of p38 mitogen-activated protein kinase in human coronary artery endothelial cells
Phosphorylated full-length BH3-interacting domain death agonist (FL-Bid) reversibly increases apoptosis initiators during mitosis, and Bid phosphorylation during mitosis-induced apoptosis initiation depends on voltage-dependent anion-selective channel protein 2 (VDAC2), suggesting that the Bcl2 family interaction network plays a crucial role in regulating the timing of apoptosis initiation [32]
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