When Bruce Uhal, professor in MSU’s Department of Physiology, began investigating the role of angiotensin-converting enzyme-2 (ACE-2) in lung injury and repair 16 years ago, he never imagined it would bring the world to a halt. ACE-2 is the main receptor, or docking molecule, for the SARS-CoV-2 virus that causes COVID-19 and led to half a million deaths in the United States.
“Starting in February 2020, I got a lot of calls and voicemails from people all over the world wanting to know how ACE-2 is controlled in the lungs and other organs,” Uhal said.
More than twenty years ago, while directing the Cardiovascular Research Institute at Michael Reese Hospital-UIC, Uhal’s lab showed that the peptide angiotensin II is involved in lung injury and repair. Unchecked angiotensin can cause hypertension, tissue fibrosis and epithelial cell death. After joining MSU in 2000, his lab was the first to describe how ACE-2, which degrades angiotensin II, protects the lungs from the injurious effects of this peptide.
When SARS emerged back in 2003, virologists and biochemists confirmed the enzyme that serves as an essential protective protein in the lungs was also the coronavirus’s preferred entry point for infection.
Then SARS-CoV-2 began surging in 2020, and ACE-2 was quickly found to be the main receptor for this coronavirus as well. At the time, Uhal was on the brink of retirement, but with so many lives at stake he instead switched to COVID-19 research, working first with Yong-Hui Zheng, professor in MSU’s Department of Microbiology and Molecular Genetics.
Read the full story on the College of Natural Science website.
