A new study has revealed a mechanism that contributes to the development of pulmonary fibrosis, which may open the door to the development of new treatments for this disease.
Pulmonary fibrosis leads to the formation of scar tissue within the lungs, which obstructs breathing and gradually leads to failure of their functions.
Researchers from the University of Technology Sydney and Monash University in Australia have found that the protein "Vitronectin" not only plays a structural role in the lungs, but also acts as a signal that changes the behavior of a type of immune cell known as macrophages, which are cells responsible for removing damaged cells and helping to repair tissues after injury.
Associate Professor Gang Liu, from the School of Life Sciences at the University of Technology Sydney, said that the natural wound-healing process is disrupted in patients with pulmonary fibrosis. Instead of repairing damaged tissue, the body begins to form scar tissue inside the lungs, leading to a decline in their function over time.
He added that the study results showed that macrophages may be reprogrammed in some cases to transform from cells that support wound healing into cells that stimulate scar formation, and that the protein "Vitronectin" represents the main factor that drives this transformation.
In order to understand this mechanism, the research team, led by Professor Katrina Binger, from the Department of Biochemistry and Molecular Biology at Monash University, developed a three-dimensional tissue culture system that mimics the natural environment inside the lung, allowing for more accurate monitoring of cell behavior.
Binger said that "Vitronectin" was previously thought to be a protein that provides structural support to lung tissue, but the study showed that it also acts as a signal that changes the way macrophages produce energy, which drives them into a state of accelerated fibrosis formation.
She added that the results recorded in three-dimensional tissue culture models matched what the researchers observed in animal models, as well as in tissue samples taken from patients with idiopathic pulmonary fibrosis, which enhances the reliability of the results.
Researchers are currently working on developing drugs that target the "vitronectin" pathway and macrophages, hoping to stop the scarring process rather than just slowing down the progression of the disease.
Liu said that understanding this mechanism represents an important step towards developing new treatments that target the direct cause of pulmonary fibrosis, expressing his hope that these results will contribute to moving the discovery from the laboratory to clinical application, giving patients more effective treatment options in the future.
