期刊
CELL
卷 184, 期 8, 页码 1990-2019出版社
CELL PRESS
DOI: 10.1016/j.cell.2021.03.005
关键词
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资金
- National Cancer Institute [T32CA071345]
- Division of Pediatric Oncology at Dana Farber training grant [T32CA136432]
- Cannonball Kids Cancer Young Investigator Award
- Mexico in Harvard Foundation-Mexican Council of Science and Technology Fellowship
- Bristol-Myers Squibb
- National Heart, Lung, and Blood Institute of the NIH [R35HL150876]
- Longfonds Stichting
- NIH [P01 AI056299, U54CA224088, R01CA213062]
- Ludwig Center at Harvard Medical School
- Paul F. Glenn Foundation for Medical Research
Human population is aging faster than ever before in history, requiring a deeper understanding of aging biology and its connection to diseases. Aging lungs face various stresses, increasing the risk of lung diseases, respiratory infections, and lung cancer.
The population is aging at a rate never seen before in human history. As the number of elderly adults grows, it is imperative we expand our understanding of the underpinnings of aging biology. Human lungs are composed of a unique panoply of cell types that face ongoing chemical, mechanical, biological, immunological, and xenobiotic stress over a lifetime. Yet, we do not fully appreciate the mechanistic drivers of lung aging and why age increases the risk of parenchymal lung disease, fatal respiratory infection, and primary lung cancer. Here, we review the molecular and cellular aspects of lung aging, local stress response pathways, and how the aging process predisposes to the pathogenesis of pulmonary disease. We place these insights into context of the COVID-19 pandemic and discuss how innate and adaptive immunity within the lung is altered with age.
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