When Anna Greka, an institute member at the Broad Institute of MIT and Harvard and a physician at Brigham and Women’s Hospital, volunteered to help care for patients with COVID-19 at the peak of Boston’s springtime surge, she saw first-hand the severity of lung damage in seriously ill patients — and how limited treatment options were.
Greka shared her clinical experience with members of her lab at Broad, which drove them to ask: was it possible to find an FDA-approved drug that could reduce lung damage? By scouring the scientific literature, the team learned that a protein called MUC1, which normally generates mucus in the lungs and other organs, plays a role in lung injury, and high levels of the protein were linked to excess mucus in the lungs of severely ill COVID-19 patients. Luckily, the Greka lab was already well acquainted with MUC1.
The team had already screened a large collection of FDA-approved drugs for compounds that block MUC1. This was part of the lab’s yearslong work in studying the cellular and molecular mechanisms underlying genetic diseases, including a rare disorder called MUC1 kidney disease (MKD), which is caused by a mutated form of the MUC1 protein. The lab thought that the data they had collected when studying MKD might provide valuable clues into how to treat MUC1-associated lung injury.
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