Timing and cell specificity of senescence drives postnatal lung development and injury
Open accessAbstract
Senescence causes age-related diseases and stress-related injury. Paradoxically, it is also essential for organismal development. Whether senescence contributes to lung development or injury in early life remains unclear. Here, we show that lung senescence occurred at birth and decreased throughout the saccular stage in mice. Reducing senescent cells at this stage disrupted lung development. In mice (<12 h old) exposed to hyperoxia during the saccular stage followed by air recovery until adulthood, lung senescence increased particularly in type II cells and secondary crest myofibroblasts. This peaked during the alveolar stage and was mediated by the p53/p21 pathway. Decreasing senescent cells during the alveolar stage attenuated hyperoxia-induced alveolar and vascular simplification. Conclusively, early programmed senescence orchestrates postnatal lung development whereas later hyperoxia-induced senescence causes lung injury through different mechanisms. This defines the ontogeny of lung senescence and provides an optimal therapeutic window for mitigating neonatal hyperoxic lung injury by inhibiting senescence.
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CDKN1A, p53 and γH2AX are upregulated in mouse and human lungs upon senescence.
“Additionally, CDKN1A, p53 and γH2AX are also upregulated in mouse and human lungs upon senescence168,169.”
From SenNet recommendations for detecting senescent cells in different tissues (2024) · cites this paper as [168]
The Results sections on p21/p53 and DNA damage (pages unavailable) report increased Cdkn1a (p21), phosphorylated p53, and γH2AX in neonatal mouse lungs after hyperoxia, but total p53 did not increase and γH2AX rose only at the early time point. The Discussion reports increased p21/γH2AX colocalization in hyperoxia-exposed human infant airways, but does not establish that all three markers are upregulated in human lungs upon senescence. (LLM, conf=0.87)
Experimental — accuracy not yet measuredIn injury-induced senescence mouse models, SASP factors including cytokines, chemokines and proteases are robustly upregulated.
“In injury-induced senescence mouse models, SASP factors including cytokines (IL-1α, IL-1β, IL-10, TNF, TNFRSF1B and TNFSF12), chemokines (CXCL2 and CXCL12) and proteases (MMP8 and MMP12) are robustly upregulated168.”
From SenNet recommendations for detecting senescent cells in different tissues (2024) · cites this paper as [168]
The Results section, “Neonatal hyperoxia induces senescence-associated secretory phenotype (SASP)” (page unavailable), reports significant increases in IL-1α, IL-1β, CXCL2, CXCL12, and TNFRSF1B in lungs of hyperoxia-exposed neonatal mice. It lists IL-10, TNF, TNFSF12, MMP8, and MMP12 among the factors tested, but does not report that those factors were significantly increased; the citing sentence overstates the finding for the full list. (LLM, conf=0.90)
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- Authors
- Yao, H., Wallace, J., Peterson, A. L., Scaffa, A., Rizal, S., Hegarty, K., Maeda, H., Chang, J. L., Oulhen, N., Kreiling, J. A., Huntington, K. E., De Paepe, M. E., Barbosa, G., & Dennery, P. A.
- Affiliations
- Brown University (US)
- Corresponding author
- Yao, Hongwei
- Dennery, Phyllis A.
- ORCID
- Venue
- Nature Communications
- Published
- 2023-01-17
- Volume
- 14
- Issue
- 1
- Pages
- 273-273
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC9845377
- OpenAlex
- W4317036030
- Cited by
- 48
- References
- 69
- Citations by year
- 2026: 12 · 2025: 18 · 2024: 13 · 2023: 5
- FWCI
- 8.84
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Nature Communications (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- U.S. Department of Health & Human Services | NIH | National Institute of General Medical Sciences (P20GM103652, P20GM109035)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Neonatal Respiratory Health Research
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Neuroscience of respiration and sleep
- Keywords
- cellular senescence, postnatal lung development, hyperoxic lung injury, neonatal hyperoxia, alveolar type II cells, p53/p21 pathway, senolytic therapy, alveolarization, lung vascularization, saccular stage
- MeSH terms
- Animals, Animals, Newborn, Lung, Pulmonary Alveoli, Hyperoxia, Mice, Lung Injury
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