Wednesday, March 1, 2017

Researchers discover link between aging, devastating lung disease

Mayo Clinic: A Mayo Clinic study has shown evidence linking the biology of aging with idiopathic pulmonary fibrosis, a disease that impairs lung function and causes shortness of breath, fatigue, declining quality of life, and, ultimately, death. Researchers believe that these findings, which appear today in Nature Communications, are the next step toward a possible therapy for individuals suffering from idiopathic pulmonary fibrosis. “Idiopathic pulmonary fibrosis is a poorly understood disease, and its effects are devastating,” says Nathan LeBrasseur, Ph.D., director, Healthy Aging and Independent Living program, Mayo Clinic Robert and Arlene Kogod Center on Aging and senior author of this study.
“Individuals with idiopathic pulmonary fibrosis express difficulty completing routine activities. There are currently no effective treatment options, and the disease leads to a dramatic decrease in health span and life span, with life expectancy after diagnosis between three to five years.”
Dr. LeBrasseur and his team, which included experts across several departments at Mayo Clinic, as well as Newcastle University Institute for Ageing and The Scripps Research Institute, studied the lung tissue of healthy individuals and of persons with mild, moderate and severe idiopathic pulmonary fibrosis. The tissue samples were made available from the Lung Tissue Research Consortium, a resource program of the National Heart, Lung, and Blood Institute, part of the National Institutes of Health (NIH). Researchers found that the markers of cellular senescence, a process triggered by damage to cells and linked to aging, were higher in individuals with idiopathic pulmonary fibrosis, and senescent cell burden increased with the progression of the disease. Then, they demonstrated that factors secreted by senescent cells could drive inflammation and aberrant tissue remodeling and fibrosis, which are hallmarks of idiopathic pulmonary fibrosis.
“We discovered that senescent cells, which accumulate in the idiopathic pulmonary fibrosis lung, are a viable source of multiple factors that drive fibrotic activation,” explains Marissa Schafer, Ph.D., a postdoctoral fellow in Dr. LeBrasseur’s lab and lead author of the study.