Fibroblasts from IPF explanted lungs have mitochondrial dysfunction and short telomeres leading to an increased senescence phenotype

Álvarez, Diana; Cárdenes, Nayra; Corey, Catherine; Hanumanthu, Vidya Sagar; D'Cunha, Hanna; Bueno, Marta; Sembrat, John; Armanios, Mary; Mora, Ana L.; Rojas, Mauricio

doi:10.1183/13993003.congress-2016.pa777

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2017

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“…Mitochondrial dysfunction and accelerated senescence are seen in IPF lung fibroblasts, but whether it reflects a distinct endotype of age-associated fibrosis is unclear (53,54). Chronic exposure to certain environmental triggers, such as cigarette smoke, may result in accumulated damage that leads to mitochondrial dysfunction and accelerated senescence of lung fibroblasts (55).…”

Section: Fibroblastsmentioning

confidence: 99%

Mitochondrial Dysfunction in Pulmonary Fibrosis

2017

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The aging of the human population has resulted in an unprecedented increase in the incidence and prevalence of age-related diseases, including those of the lung. Idiopathic pulmonary fibrosis is a disease of aging, and is characterized by a progressive decline in lung function and high mortality. Recent studies suggest that mitochondrial dysfunction, which can accompany aging phenotypes, may contribute to the pathogenesis of idiopathic pulmonary fibrosis. In this review, we explore current evidence for mitochondrial dysfunction in alveolar epithelial cells, fibroblasts, and immune cells that participate in the fibrotic process. Further, the fates of these cell populations and the potential to target mitochondrial dysfunction as a therapeutic strategy are discussed.

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Section: Fibroblastsmentioning

confidence: 99%