Aldehyde metabolism governs resilience of mucociliary clearance to air pollution exposure

Shinjyo, Noriko; Kimura, Haruna; Yoshihara, Tomomi et al.

Journal of Clinical Investigation, 2025, 135(14), e191276

Number of Access:7（2025-11-13 23:50 Counts）

Identifier to cite or link to this item: https://hdl.handle.net/11094/102919

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Title
Aldehyde metabolism governs resilience of mucociliary clearance to air pollution exposure
Creator
NRID
1000060794039 1000060794039
ORCID
0000-0003-4501-4513 0000-0003-4501-4513
researchmap permalink
Noriko_Shinjyo Noriko_Shinjyo
Scopus Author ID
6506391838 6506391838
CreatorName
Shinjyo, Noriko
Scopus Author ID
59377626200 59377626200
CreatorName
Kimura, Haruna
Scopus Author ID
58140535000 58140535000
CreatorName
Yoshihara, Tomomi
NRID
1000030511894 1000030511894
CreatorName
Suzuki, Jun
NRID
1000000714536 1000000714536
CreatorName
Yamaguchi, Masaya
NRID
1000050273694 1000050273694
researchmap permalink
read0185239 read0185239
Scopus Author ID
7201354003 7201354003
CreatorName
Kawabata, Shigetada
NRID
1000050522124 1000050522124
ORCID
0000-0002-1913-7280 0000-0002-1913-7280
researchmap permalink
7000018117 7000018117
Scopus Author ID
36917266300 36917266300
CreatorName
Okabe, Yasutaka
Description
Shinjyo N., Kimura H., Yoshihara T., et al. Aldehyde metabolism governs resilience of mucociliary clearance to air pollution exposure. Journal of Clinical Investigation 135(14), e191276 (2025); https://doi.org/10.1172/JCI191276.
Abstract
Air pollution is a serious environmental threat to public health; however, the molecular basis underlying its detrimental effects on respiratory fitness remains poorly understood. Here, we showed that exposure to particulate matter ≤ 2.5 μm (PM₂.₅), a substantial fraction of air pollutants, induced the generation of reactive aldehyde species in the airway. We identified aldehyde dehydrogenase 1A1 (ALDH1A1), which was selectively expressed in airway epithelium, as an enzyme responsible for detoxifying these reactive aldehyde species. Loss of ALDH1A1 function resulted in the accumulation of aldehyde adducts in the airway, which selectively impaired mucociliary clearance (MCC), a critical defense mechanism against respiratory pathogens. Thus, ALDH1A1-deficient mice pre-exposed to PM₂.₅ exhibited increased susceptibility to pneumonia. Conversely, pharmacological enhancement of ALDH1A1 activity promoted the restoration of MCC function. These findings elucidate the critical role of aldehyde metabolism in protecting against PM₂.₅ exposure, offering a potential target to mitigate the negative health consequences of air pollution.
Publisher
American Society for Clinical Investigation
Source Title
Journal of Clinical Investigation
Volume (Issue)
135(14)
Page
e191276
Date of Issued
2025-07-15
Language
English
Handle URL
https://hdl.handle.net/11094/102919
PISSN
00219738
eISSN
15588238
Relation.isIdenticalTo
DOI (Publisher Version)
https://doi.org/10.1172/JCI191276
Access Rights
open access
CopyRight
This article is licensed under a Creative Commons Attribution 4.0 International License.
oaire:version
Version of Record
Category
学術雑誌論文 Journal Article