Good news!
It is really disgusting that the American Association for the Advancement of Science (AAAS) uses "person" or "people" to refer to a pregnant woman! To date there are no pregnant transgender women!
"In about a tenth of all pregnancies, danger strikes sometime after 20 weeks. The pregnant person’s blood pressure rises, and if it stays too high for too long, it can cause organ damage and even kill them. This condition, known as preeclampsia, happens with essentially no warning. But now, scientists have pinpointed an apparent cause, which could lead to earlier notice that the condition is developing or—hopefully—ways of preventing it altogether.
Researchers compared placental tissues from people who did and didn’t experience preeclampsia prior to delivery, zeroing in on cells in a layer called the syncytiotrophoblast, which helps shield the fetus from immune attack. In people with preeclampsia, these cells exhibited higher levels of stress, and the team noticed increased activity of certain proteins involved in hormonal signaling—a clue as to where that stress might be coming from. Sure enough, when the team engineered mice to have hyperactive versions of these proteins in this placental layer, the mice developed all the usual signs of preeclampsia. And even more excitingly, a drug known to reduce cellular stress reduced these symptoms. ..."
From the abstract:
"Syncytiotrophoblast stress is theorized to drive development of preeclampsia, but its molecular causes and consequences remain largely undefined. Multiple hormones implicated in preeclampsia signal via the Gαq cascade, leading to the hypothesis that excess Gαq signaling within the syncytiotrophoblast may contribute. First, we present data supporting increased Gαq signaling and antioxidant responses within villous and syncytiotrophoblast samples of human preeclamptic placenta. Second, Gαq was activated in mouse placenta using Cre-lox and DREADD methodologies. Syncytiotrophoblast-restricted Gαq activation caused hypertension, kidney damage, proteinuria, elevated circulating proinflammatory factors, decreased placental vascularization, diminished spiral artery diameter, and augmented responses to mitochondrial-derived superoxide. Administration of the mitochondrial-targeted antioxidant Mitoquinone attenuated maternal proteinuria, lowered circulating inflammatory and anti-angiogenic mediators, and maintained placental vascularization. These data demonstrate a causal relationship between syncytiotrophoblast stress and the development of preeclampsia and identify elevated Gαq signaling and mitochondrial reactive oxygen species as a cause of this stress."
Fig. 3. Evidence of increased Gαq signaling and an oxidative defense response in human syncytiotrophoblast cells during preeclampsia.
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