About 10% of lung transplants in the U.S. are going to COVID-19 patients — and researchers are finding out why.

Researchers from Michigan State University and CoreWell Health, in collaboration with the Cleveland Clinic, have made significant progress in understanding pulmonary complications after COVID-19 infection.

The study was led by Xiaopeng Li of Michigan State University, Reda Girgis of CoreWell Health and Kun Li of the Florida Center for Research and Innovation at the Cleveland Clinic. Published of American Journal of Respiratory Cell and Molecular Biology It also highlights the role of a gene called ATP12A in promoting lung damage and excessive mucus production after COVID-19 infection.

COVID-19 infection may activate this gene in the lungs, leading to progressive lung scarring and ultimately the need for lung transplantation. This collaborative study investigated the biological factors behind the increased lung transplant rates in patients with pulmonary fibrosis after COVID-19 infection. Currently, nearly 10% of lung transplants in the United States are performed on COVID-19 patients, according to data from the United Nations Network for Organ Donation (UNOS).

“Understanding why and how some people develop severe lifelong complications is critical for developing more effective treatments for lung injury after COVID-19 infection,” said Xiaopeng Li, associate professor in the Department of Pediatrics and Human Development at Michigan State University's College of Human Medicine.

In collaboration with Kun Li, Xiaopeng Li investigated the expression of ATP12A in lung samples from patients who had undergone lung transplants. Clinical samples provided by Reda Girgis, medical director of the Lung Transplant Program at CoreWell Health and professor at Michigan State University, found elevated levels of ATP12A in patients with post-COVID-19 pulmonary fibrosis that were similar to fibrosis unrelated to COVID-19.

“At the Cleveland Clinic, we have confirmed that COVID-19 infection directly increases ATP12A levels, contributing to pulmonary fibrosis,” Kun Lee noted.

“This discovery lays the foundation for potential therapeutic interventions aimed at benefiting all pulmonary fibrosis patients, regardless of the origin of their condition. The researchers' next step is to elucidate how infection increases ATP12A levels and how this contributes to pulmonary fibrosis, paving the way for future treatment improvements.”