Mechanistic links between aging and lung fibrosis.
Our understanding of the biology of aging has advanced significantly in recent years. This has resulted in the recent formulation of the "hallmarks of aging" that include genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication. Idiopathic pulmonary fibrosis (IPF) is a progressive and fatal lung disease that results from the accumulation of scar tissue in the lungs of affected individuals. IPF is a disease of aging that most commonly affects human subjects older than 60 years of age. While progress has been made in elucidating key pathological processes in IPF, the relationship of these processes to those that occur during aging are not well defined. In this review, we explore existing and emerging paradigms in the pathogenesis of IPF in light of the recently defined hallmarks of aging.
Division of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Alabama at Birmingham, 429 THT, 1900 University Blvd., Birmingham, AL, 35294-0006, USA, vjthan@uab.edu.
Victor J
VJ
Thannickal
D000367:Age Factors; D000375:Aging / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D000818:Animals; D002450:Cell Communication; D016922:Cellular Senescence; D044127:Epigenesis, Genetic; D042822:Genomic Instability; D006801:Humans; D054990:Idiopathic Pulmonary Fibrosis / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D008928:Mitochondria / Q000378:metabolism / Q000473:pathology; D009752:Nutritional Status; D059748:Proteolysis; D013234:Stem Cells / Q000378:metabolism / Q000473:pathology; D059505:Telomere Homeostasis