Intersection of Inflammation and Senescence in the Aging Lung Stem Cell Niche - PubMed (original) (raw)

Review

Intersection of Inflammation and Senescence in the Aging Lung Stem Cell Niche

Nancy C Allen et al. Front Cell Dev Biol. 2022.

Abstract

Aging is the final stage of development with stereotyped changes in tissue morphology. These age-related changes are risk factors for a multitude of chronic lung diseases, transcending the diverse pathogenic mechanisms that have been studied in disease-specific contexts. Two of the hallmarks of aging include inflammation and cellular senescence, which have been attributed as drivers of age-related organ decline. While these two age-related processes are often studied independently in the same tissue, there appears to be a reciprocal relationship between inflammation and senescence, which remodels the aging tissue architecture to increase susceptibility to chronic diseases. This review will attempt to address the "chicken or the egg" question as to whether senescence drives inflammation in the aging lung, or vice versa, and whether the causality of this relationship has therapeutic implications for age-related lung diseases.

Keywords: SASP; aging; inflammation; senescence; stem cell niche.

Copyright © 2022 Allen, Reyes, Lee and Peng.

PubMed Disclaimer

Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

FIGURE 1

FIGURE 1

Positive inflammatory feedback loop between senescent cells and the immune system in the aging lung stem cell niche. With age, senescent cells accumulate within the lung parenchyma and secrete SASP factors that both recruit immune cells and alter immune cell function. Subsequently, recruited immune cells secrete cytokines that reinforce and potentially even propagate cellular senescence. The pro-inflammatory environment created by this positive feedback loop contributes to age-related alterations in lung epithelial stem cell function.

References

    1. Abdel-Daim M. M., Moustafa Y. M., Umezawa M., Ramana K. V., Azzini E. (2017). Applications of Antioxidants in Ameliorating Drugs and Xenobiotics Toxicity: Mechanistic Approach. Oxidative Med. Cell. Longev. 2017, 4565127. 10.1155/2017/4565127 -DOI -PMC -PubMed
    1. Acosta J. C., Banito A., Wuestefeld T., Georgilis A., Janich P., Morton J. P., et al. (2013). A Complex Secretory Program Orchestrated by the Inflammasome Controls Paracrine Senescence. Nat. Cell. Biol. 15, 978–990. 10.1038/ncb2784 -DOI -PMC -PubMed
    1. Acosta J. C., O'Loghlen A., Banito A., Guijarro M. V., Augert A., Raguz S., et al. (2008). Chemokine Signaling via the CXCR2 Receptor Reinforces Senescence. Cell. 133, 1006–1018. 10.1016/j.cell.2008.03.038 -DOI -PubMed
    1. Adams T. S., Schupp J. C., Poli S., Ayaub E. A., Neumark N., Ahangari F., et al. (2020). Single-cell RNA-Seq Reveals Ectopic and Aberrant Lung-Resident Cell Populations in Idiopathic Pulmonary Fibrosis. Sci. Adv. 6, eaba1983. 10.1126/sciadv.aba1983 -DOI -PMC -PubMed
    1. Alder J. K., Chen J. J.-L., Lancaster L., Danoff S., Su S.-c., Cogan J. D., et al. (2008). Short Telomeres Are a Risk Factor for Idiopathic Pulmonary Fibrosis. Proc. Natl. Acad. Sci. U.S.A. 105, 13051–13056. 10.1073/pnas.0804280105 -DOI -PMC -PubMed

Publication types

LinkOut - more resources