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. 2020 Feb 11;11:98. doi: 10.3389/fphys.2020.00098

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Copyright © 2020 Raguema, Moustadraf and Bertagnolli.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Placental apoptosis mechanisms. (A) Extrinsic apoptosis pathway activation in maternal immune cells stimulated by trophoblasts producing FASL. (B) Extrinsic apoptosis activation in trophoblasts stimulated by FASL produced by the maternal immune system and intrinsic pathway activated by environmental stress such as hypoxia and DNA damage. FAS, FAS receptor; FASL, FAS ligand; FADD, Fas-associated protein with death domain; C-FLIP, cellular FLICE (FADD-like IL-1β-converting enzyme)-inhibitory protein; P53, apoptosis inductor; BCL-2, B-cell lymphoma 2; BAX, BCL2-associated X apoptosis regulator; Mdm2, Human mouse double minute 2; Bid, BH3 interacting-domain death agonist; tBid, truncated p15 BID; Apaf-1, apoptotic protease activating factor 1.