Groundbreaking Study Reveals Why COVID-19 Patients Make Up Nearly 10% of U.S. Lung Transplants

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East Lansing, MI - A groundbreaking new study by Michigan State University (MSU), Corewell Health, and the Cleveland Clinic has uncovered critical insights into the rising number of lung transplants among COVID-19 patients. Published in the American Journal of Respiratory Cell and Molecular Biology, the research highlights the role of the gene ATP12A in causing lung damage and excessive mucus production in individuals who have experienced severe post-COVID-19 complications.

The Impact of COVID-19 on Lung Transplantation

According to data from the United Network for Organ Sharing (UNOS), nearly 10% of all lung transplants in the U.S. now go to patients suffering from post-COVID pulmonary fibrosis. This condition, which results in progressive scarring of the lungs, has become one of the most serious long-term effects of the COVID-19 virus.

The study, led by Xiaopeng Li of MSU, Reda Girgis of Corewell Health, and Kun Li of Cleveland Clinic’s Florida Research and Innovation Center, examined how COVID-19 triggers the activation of the ATP12A gene, which plays a pivotal role in the development of lung fibrosis. This gene causes the lungs to produce excessive amounts of mucus and promotes scarring, which, in many cases, can only be resolved through a lung transplant.

“Understanding how and why some individuals develop severe lifelong complications is critical to developing more effective post-COVID lung damage treatment,” said Xiaopeng Li, associate professor in MSU’s College of Human Medicine’s Department of Pediatrics and Human Development.

Research Findings on ATP12A and Lung Fibrosis

In collaboration with Kun Li, the team analyzed lung samples from patients undergoing lung transplantation due to post-COVID pulmonary fibrosis. The research confirmed that the ATP12A gene is significantly elevated in individuals with this condition, much like other forms of lung fibrosis unrelated to COVID-19.

“At Cleveland Clinic, we confirmed COVID-19 infection directly caused ATP12A levels to increase and contributed to pulmonary fibrosis,” said Kun Li.

The elevated expression of ATP12A after COVID-19 infection explains why certain patients experience severe lung damage, ultimately requiring transplantation. This discovery not only sheds light on the growing need for lung transplants in COVID-19 patients but also opens the door to potential new therapeutic interventions for all patients suffering from pulmonary fibrosis, regardless of its cause.

A Path Toward Better Treatment for Post-COVID Lung Damage

The next phase of this critical research will focus on understanding how COVID-19 infection elevates ATP12A levels and contributes to lung scarring. The hope is that by targeting this gene, scientists can develop better treatments to prevent the onset of pulmonary fibrosis and reduce the need for lung transplants.

The findings from this collaboration are a significant step forward in addressing the long-term health impacts of COVID-19 and could ultimately help improve the quality of life for patients who continue to struggle with post-COVID lung complications.

As the team moves forward with their research, their work could pave the way for the development of new therapies to treat pulmonary fibrosis, offering hope to thousands of patients across the country.