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Genome study suggests new strategies for understanding and treating pulmonary fibrosis
Date:4/19/2013

variations in this gene may lead to pulmonary fibrosis by interfering with mucosal defense, repair of lung alveoli or direct toxicity to cells.

The researchers also found stronger evidence for the role of telomeres, a protective section of DNA located at the tips of chromosomes. Shorter telomeres are associated with a reduced ability to divide and premature cell death. Previously, two rare genetic mutations had been associated with some forms of pulmonary fibrosis. The research team found common variants in and near those two genes, and a common variant in another gene.

The researchers also identified three genes associated with connections that hold adjoining cells together, known as cell-cell adhesion. Impaired cell-cell adhesion can lead to lost tissue integrity.

These findings support the researchers' belief that pulmonary fibrosis may be influenced by different genes in different people. Careful genotyping could identify different forms of the disease, allowing for more effective, individualized therapy.

The research was supported by the National Heart, Lung and Blood Institute (NHLBI). "In addition to expanding the library of genetic changes that can underlie pulmonary fibrosis, this study's findings demonstrate that both rare and common genetic variants contribute significantly to pulmonary fibrosis risk," said James Kiley, PhD, Director of NHLBI's Division of Lung Diseases. "A key next step for research is figuring out how these genetic variants work with environmental factors in the development of the disease."


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Contact: William Allstetter
allstetterw@njhealth.org
303-398-1002
National Jewish Health
Source:Eurekalert

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