Fig. 5: PTRH2-regulated cardioprotection during pregnancy.

The heart undergoes hypertrophy to account for the augmented mechanical load required during pregnancy to compensate for the increased blood flow to the fetus. This places extreme mechanical stresses on the heart. In the healthy heart such pregnancy associated stresses activate cardiomyocyte pro-survival pathways, including PTRH2. Upon the loss of PTRH2 expression, PTRH2-mediated cardio-protective signals are not activated, promoting increased caspase 3 activity and cardiomyocyte apoptosis that leads to PPCM progression to heart failure postpartum. Inhibiting caspase 3 blocks PPCM progression to heart failure. Schematic was created using BioRender (https://biorender.com).