Pregnancy is meant to be a season of renewal, yet for some women the second half brings a rise in blood pressure that can strain both mother and child, sometimes with lasting consequences. Until now, doctors have had little to offer beyond bringing the birth forward. A team from Massachusetts General Hospital and the Broad Institute, working with genetic data from more than 600,000 people, has begun to trace the hidden machinery behind these conditions, pointing to six blood proteins that appear to either drive the disorders or guard against them. The discovery is an early map rather than a de
Six Blood Proteins Linked to Pregnancy Hypertension Disorders, Pointing to Possible New Targets
Preeclampsia and related disorders carry considerable short- and long-term risks for both mother and child, with limited treatment beyond expedited delivery.
Treatment options, other than expedited delivery, remain limited.
Mark
Start with the basics. What did this team actually find?
Mimi
Six blood proteins whose genetically predicted levels appear tied to the risk of hypertensive disorders of pregnancy. Some likely contribute to risk, and some likely protect.
Mark
Which ones?
Mimi
CD40, cystatin B, eosinophil cationic protein, galectin-3, heat shock protein 27, and N-terminal pro-B type natriuretic peptide.
Mark
Why does that matter clinically?
Mimi
Right now, apart from expedited delivery, treatment options are limited. These proteins span blood vessel regulation, inflammation, and immunity, so they hint at several biological routes into the disease.
Luke
I want to be careful with the word causal. The source says the evidence is strong and the proteins likely contribute or protect. That's a strong signal, not proof of mechanism.
Mark
Fair. How big was the dataset?
Mimi
Genetic data from more than 600,000 individuals, and the question was whether inherited tendencies toward higher or lower protein levels shifted a woman's risk.
Luke
Worth saying what we don't have. The reporting doesn't give effect sizes, doesn't say which proteins raise risk and which lower it, and doesn't say how many of those 600,000 were pregnant women.
Mark
So what's the honest next step?
Mimi
Honigberg says animal models first, then human trials if the proteins look promising.
Luke
And that's a long road. Calling these treatment targets is his hope, not a result.
El Pulso
- Blood pressure rises in the later stages of pregnancy, threatening both mother and child with short- and long-term harm.
- Treatment options remain narrow, with early delivery still the main response once the disorder takes hold.
- Researchers used inherited genetic variation across more than 600,000 people to test which blood proteins actually cause or shield against the condition.
- Six proteins linked to blood vessels, inflammation and immunity emerged as likely players, including CD40, galectin-3 and heat shock protein 27.
- The findings now must pass through animal studies before any human trial, so no treatment exists yet and none is imminent.
Pregnancy is meant to be a season of renewal, yet for some women the second half brings a rise in blood pressure that can strain both mother and child, sometimes with lasting consequences. Until now, doctors have had little to offer beyond bringing the birth forward. A team from Massachusetts General Hospital and the Broad Institute, working with genetic data from more than 600,000 people, has begun to trace the hidden machinery behind these conditions, pointing to six blood proteins that appear to either drive the disorders or guard against them. The discovery is an early map rather than a destination, and whether these signposts lead to new treatments will depend on the slow, careful work still ahead.
Preeclampsia and the other hypertensive disorders of pregnancy are marked by high blood pressure in the second half of pregnancy, sometimes accompanied by damage to organs. The risks reach both mother and baby, now and for years afterward, and medicine has offered little beyond delivering the child sooner.
A team led by researchers at Massachusetts General Hospital and the Broad Institute, publishing in JAMA Cardiology, has started to look underneath the condition. They asked whether inherited tendencies toward higher or lower levels of particular blood proteins change a woman's risk. Because the method begins with genetic variation, it comes closer to cause and effect than a simple comparison of blood samples could.
Across more than 600,000 people, the analysis flagged six proteins that likely contribute to these disorders or protect against them: CD40, cystatin B, eosinophil cationic protein, galectin-3, heat shock protein 27, and N-terminal pro-B type natriuretic peptide. Senior author Michael C. Honigberg, a cardiologist at MGH and Harvard Medical School, sees pathways in blood vessel regulation, inflammation and immunity, and believes some of these proteins could one day become therapeutic targets.
He is clear that this is not yet a treatment, and no drug has been proposed. The next step is animal research, and only if those experiments are promising would human trials follow. The work was supported by the National Institutes of Health and the American Heart Association.
Preeclampsia and the other hypertensive disorders of pregnancy are defined by high blood pressure in the second half of pregnancy, with or without organ dysfunction. They carry considerable risks for both mother and child, in the short term and the long term. Beyond delivering the baby sooner, treatment options remain limited.
A team led by researchers at Massachusetts General Hospital and the Broad Institute has now pointed to several blood proteins that may help explain how these conditions arise. Their work, published in JAMA Cardiology, found strong evidence that certain proteins play either a causal or a protective role.
The study drew on genetic data from more than 600,000 individuals. The investigators asked a specific question: does a genetic predisposition to higher or lower levels of particular proteins in the bloodstream change a woman's risk of developing a hypertensive disorder of pregnancy? Because the approach starts from inherited variation in protein levels, it is designed to get closer to cause and effect than a simple comparison of blood samples would. The keywords attached to the work name the method as Mendelian randomization.
The analysis identified six proteins involved in cardiovascular and inflammatory processes that likely contribute to these conditions or protect against them. They are CD40, cystatin B, eosinophil cationic protein, galectin-3, heat shock protein 27, and N-terminal pro-B type natriuretic peptide.
Michael C. Honigberg, a cardiologist and researcher at MGH and assistant professor of medicine at Harvard Medical School, is the senior author. He said the findings offer new insight into the biology of these disorders and suggest that several pathways are involved in their development, including blood vessel regulation, inflammation, and immunity. In his view, some of the proteins could become therapeutic targets.
He was explicit about the next steps. Those proteins, he said, should be investigated further in animal models and, if they prove promising, ultimately in human trials. Nothing in the study amounts to a treatment, and no drug is yet proposed.
The author list is long. It includes Art Schuermans, Buu Truong, Maddalena Ardissino, Rohan Bhukar, Eric Slob, Tetsushi Nakao, Jacqueline Dron, Aeron Small, So Mi Jemma Cho, Zhi Yu, Whitney Hornsby, Adam Butterworth, Stephen Burgess, James Januzzi Jr, and Pradeep Natarajan, among others. The work was supported by the National Institutes of Health and the American Heart Association.
What to watch is whether laboratory work in animal models bears out any of the six proteins. Only then would human trials come into view, in a field where delivery remains the main option once these conditions take hold.
Citas Notables
Some of the proteins could serve as potential therapeutic targets and should be investigated further in animal models and, if promising, in human trials.— Michael C. Honigberg, MD, MPP, senior author, MGH and Harvard Medical School
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