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Abstract

Aging and Pulmonary Fibrosis

VOLUME 68 - NUMBER 2 / March - April (Review articles)

Moisés Selman, Deputy Editor, RIC, and Instituto Nacional de Enfermedades Respiratorias "Ismael Cosío Villegas" (INER), Mexico City, Mexico
Ivette Buendía-Roldán, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, SSA, Mexico City, Mexico. Deputy Editors of Revista de Investigación Clínica
Annie Pardo, Facultad de Ciencias, Universidad Nacional Autónoma de México, Mexico City, Mexico

Idiopathic pulmonary fibrosis is a chronic, progressive, and usually fatal lung disorder of unknown etiology. The disease likely results from the interaction of genetic susceptibility architecture, environmental factors such as smoking, and an abnormal epigenetic reprogramming that leads to a complex pathogenesis. Idiopathic pulmonary fibrosis occurs in middle-aged and mainly elderly adults, and in this context age has emerged as its strongest risk factor. However, the mechanisms linking it to aging are uncertain. Recently, nine molecular and cellular hallmarks of aging have been proposed: genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication. In this review, we provide an overview of these molecular mechanisms and their involvement in the pathogenesis of idiopathic pulmonary fibrosis, while emphasizing that the studies on this disease are few and the findings are not definitive.

Keywords: Aging. Lung fibrosis. Senescence. Telomeres.

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