A research team at Hannover Medical School may have cracked the code to slowing the development of pulmonary fibrosis and possibly reversing inflammatory damage. Results of its latest study, “Telomerase modRNA Offers a Novel RNA-Based Approach to Treat Human Pulmonary Fibrosis,” were published in the journal Aging Cell.
Christian Bär, PhD, research group leader at the Institute for Molecular and Translational Therapy Strategies at Hannover Medical School (MHH), and Shambhabi Chatterjee, PhD, led the team’s investigation of the role of telomerase in idiopathic pulmonary fibrosis (IPF).
Telomeres are protective caps at the end of chromosomes. Over time, telomeres progressively shorten until cells stop dividing and the tissue ages. Pulmonary fibrosis causes this process to occur prematurely, which increases inflammatory and chromosomal damage.
In the study, the MHH team increased telomerase activity in human lung cells and tissue, which resulted in significantly slowing cell aging and fibrosis development. This confirms that the telomerase subunit — telomerase reverse transcriptase (TERT) — has a critical role in extending the length of telomeres and improving the disease.
The researchers introduced messenger RNA (mRNA) containing the building block for TERT into human lung connective tissue cells. The approach generated excess telomerase activity that improved the biomarkers for aging and pulmonary fibrosis.
The team administered the TERT blueprint using modified mRNA (modRNA) technology to ensure the immune system would accept it and not trigger a harmful response. The method is safer than conventional gene therapy, as the genes only remain in the body for a few days, said Dr. Bär in an MHH news article.
“According to our results, TERT therapy is a promising approach to improving the health of lung cells and slowing down and perhaps even reversing the development of fibrosis,” he said.
The researchers noted that packing TERT in lipid nanoparticles means the modRNA could eventually be inhaled.
