Literature DB >> 23982440

Cellular senescence in normal and premature lung aging.

B Bartling1.   

Abstract

The incidence of chronic respiratory diseases (e.g., chronic obstructive pulmonary disease, COPD) and interstitial lung diseases (e.g., pneumonia and lung fibrosis) increases with age. In addition to immune senescence, the accumulation of senescent cells directly in lung tissue might play a critical role in the increased prevalence of these pulmonary diseases. In the last couple of years, detailed studies have identified the presence of senescent cells in the aging lung and in diseased lungs of patients with COPD and lung fibrosis. Cellular senescence has been shown for epithelial cells of bronchi and alveoli as well as mesenchymal and vascular cells. Known risk factors for pulmonary diseases (cigarette smoke, air pollutions, bacterial infections, etc.) were identified in experimental studies as being possible mediators in the development of cellular senescence. The present findings indicate the importance of cellular senescence in normal lung aging and in premature aging of the lung in patients with COPD, lung fibrosis, and probably other respiratory diseases.

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Year:  2013        PMID: 23982440     DOI: 10.1007/s00391-013-0543-3

Source DB:  PubMed          Journal:  Z Gerontol Geriatr        ISSN: 0948-6704            Impact factor:   1.281


  68 in total

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Review 4.  Viral infection and aging as cofactors for the development of pulmonary fibrosis.

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Journal:  Expert Rev Respir Med       Date:  2010-12       Impact factor: 3.772

5.  Accelerated epithelial cell senescence in IPF and the inhibitory role of SIRT6 in TGF-β-induced senescence of human bronchial epithelial cells.

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Journal:  Am J Physiol Lung Cell Mol Physiol       Date:  2010-12-17       Impact factor: 5.464

Review 6.  Tobacco, inflammation, and respiratory tract cancer.

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7.  In vitro cytotoxicity and mutagenicity of mainstream waterpipe smoke and its functional consequences on alveolar type II derived cells.

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8.  Shortened telomeres in circulating leukocytes of patients with chronic obstructive pulmonary disease.

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Journal:  Am J Respir Crit Care Med       Date:  2009-01-29       Impact factor: 21.405

Review 9.  ATM, ATR and DNA-PK: initiators of the cellular genotoxic stress responses.

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  7 in total

1.  Aging-mechanisms, models, and translation.

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Journal:  Hum Cell       Date:  2015-02-18       Impact factor: 4.174

3.  Reduced proliferation capacity of lung cells in chronic obstructive pulmonary disease.

Authors:  Babett Bartling; Hans-Stefan Hofmann
Journal:  Z Gerontol Geriatr       Date:  2018-02-22       Impact factor: 1.281

4.  Downregulation of DUOX1 function contributes to aging-related impairment of innate airway injury responses and accelerated senile emphysema.

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5.  Increased expression of TROP2 in airway basal cells potentially contributes to airway remodeling in chronic obstructive pulmonary disease.

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6.  Serum from patients with chronic obstructive pulmonary disease induces senescence-related phenotype in bronchial epithelial cells.

Authors:  Barbara Kuźnar-Kamińska; Justyna Mikuła-Pietrasik; Anna Witucka; Aleksandra Romaniuk; Natalia Konieczna; Błażej Rubiś; Krzysztof Książek; Andrzej Tykarski; Halina Batura-Gabryel
Journal:  Sci Rep       Date:  2018-08-28       Impact factor: 4.379

Review 7.  Cellular senescence in lymphoid organs and immunosenescence.

Authors:  Vivekananda Budamagunta; Thomas C Foster; Daohong Zhou
Journal:  Aging (Albany NY)       Date:  2021-08-12       Impact factor: 5.682

  7 in total

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