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Thannickal, V.J.* ; Murthy, M.* ; Balch, W.E.* ; Chandel, N.S.* ; Meiners, S. ; Eickelberg, O. ; Selman, M.* ; Pardo, A.* ; White, E.S.* ; Levy, B.D.* ; Busse, P.J.* ; Tuder, R.M.* ; Antony, V.B.* ; Sznajder, J.I.* ; Budinger, G.R.*

Blue journal conference : Aging and susceptibility to lung disease.

Am. J. Respir. Crit. Care Med. 191, 261-269 (2015)
Verlagsversion DOI
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Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
The aging of the population in the United States and throughout the developed world has increased morbidity and mortality attributable to lung disease, while the morbidity and mortality from other prevalent diseases has declined or remained stable. Recognizing the importance of aging in the development of lung disease, the American Thoracic Society (ATS) highlighted this topic as a core theme for the 2014 annual meeting. The relationship between aging and lung disease was discussed in several oral symposiums and poster sessions at the annual ATS meeting. In this article, we used the input gathered at the conference to develop a broad framework and perspective to stimulate basic, clinical, and translational research to understand how the aging process contributes to the onset and/or progression of lung diseases. A consistent theme that emerged from the conference was the need to apply novel, systems-based approaches to integrate a growing body of genomic, epigenomic, transcriptomic, and proteomic data and elucidate the relationship between biologic hallmarks of aging, altered lung function, and increased susceptibility to lung diseases in the older population. The challenge remains to causally link the molecular and cellular changes of aging with age-related changes in lung physiology and disease susceptibility. The purpose of this review is to stimulate further research to identify new strategies to prevent or treat age-related lung disease.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Review
Schlagwörter Idiopathic Pulmonary-fibrosis; Stem-cells; Extracellular-matrix; United-states; Alpha(1)-antitrypsin Deficiency; Cellular Senescence; Mitochondrial-dna; Telomere Length; Gene-expression; Virus-infection
ISSN (print) / ISBN 1073-449X
e-ISSN 1535-4970
Quellenangaben Band: 191, Heft: 3, Seiten: 261-269 Artikelnummer: , Supplement: ,
Verlag American Thoracic Society
Verlagsort New York
Begutachtungsstatus Peer reviewed