For more than a century, preeclampsia has resisted a simple explanation. The condition is a sudden, dangerous rise in blood pressure during pregnancy, and it can put both mother and baby at serious risk. It affects as many as one in 10 pregnancies worldwide and 5% to 8% of pregnancies in the United States. Doctors have long been able to describe what preeclampsia looks like. They have not been able to agree on what causes it.

That is because preeclampsia does not show up the same way twice. In some patients, it appears as damaged blood vessels. In others, it shows up as inflammation, or as scarring in the placenta itself. For years, researchers treated these as three separate puzzles, each with its own theory and its own dead ends.

A team at the University of Michigan, led by Dr. Johann Gudjonsson and research assistant professor Olesya Plazyo, found a way to trace all three back to a single source: a gene network centered on a molecule called VGLL3.

The discovery began almost by accident, in an entirely different field. Gudjonsson’s lab had been studying VGLL3 in skin conditions and noticed that it was strongly elevated in autoimmune diseases known to raise the risk of preeclampsia. A hallway conversation with an obstetrics colleague turned that observation into a hypothesis worth testing. What if the same gene driving those autoimmune patterns was also driving preeclampsia?

It was. Using detailed genetic sequencing of human placental tissue, the team found VGLL3 elevated in preeclamptic pregnancies, and found it capable of disrupting blood vessel development, triggering inflammation and altering placental tissue all at once. The team tested the theory two ways. In pregnant mice, removing the VGLL3 gene allowed for entirely normal pregnancies. In donated human placental tissue from women with preeclampsia, targeting VGLL3 reversed the very features doctors have struggled to treat for generations, without harming the tissue’s ability to support a healthy pregnancy. The findings were published in the journal Circulation.

For Dr. Ashley Hesson, an OB-GYN on the research team and associate director of U-M’s Cardio-Obstetrics Program, the work carries personal weight. She has had preeclampsia herself, and she understands firsthand what it means to hand a patient answers that medicine has not had.

There is no approved VGLL3-targeting treatment yet, and there will not be one soon. Getting from a laboratory discovery to a bedside therapy takes years of additional research, funding and clinical trials. But for the first time, researchers have a specific molecular target and a real reason to believe it can be safely addressed without harming mother or child.

That is what sustained research funding makes possible: not an instant cure, but the slow, careful work of turning a century-old mystery into a solvable problem. Michigan’s research universities are where that work happens.

Michigan’s research universities are also an economic engine, generating $51.4 billion in annual economic activity, 7.1% of the state’s GDP. A call for cuts to university research is a call to cut the lifesaving discoveries and the economic benefits Michigan residents have relied on for generations.

Discover how Michigan’s research universities are solving real problems across the state:

Michigan State University: https://msu.edu/researchforyou

Michigan Technological University: https://www.mtu.edu/research/

University of Michigan: https://looktomichigan.umich.edu/

Wayne State University: https://wayne.edu/research-impact