Evidence map›Paper›PMID 42491861›Full record

ArticleiScience2026

SIRT3 deficiency drives alveolar epithelial mitochondrial dysfunction in bronchopulmonary dysplasia via PDHA1 hyperacetylation.

Cong Zhao, Hua Peng, Yalan Liu, Yan Chen, Chao Tong, Qianxue Zheng, Ziang Liu, Chunyan Chen, Jiayun Zhang, Wenbo Zhu and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors.

Cong ZhaoDepartment of Pediatrics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China.
Hua PengDepartment of Pediatrics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China.
Yalan LiuDepartment of Pediatrics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China.
Yan ChenDepartment of Pediatrics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China.
Chao TongDepartment of Pediatrics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China.
Qianxue ZhengDepartment of Pediatrics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China.
Ziang LiuDepartment of Pediatrics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China.
Chunyan ChenDepartment of Pediatrics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China.
Jiayun ZhangDepartment of Pediatrics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China.
Wenbo ZhuDepartment of Pediatrics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China.
Xu GuoDepartment of Pediatrics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China.
Shiyi JiangDepartment of Pediatrics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China.
Lin WangDepartment of Pediatrics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China.
Jie LiuDepartment of Pediatrics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bronchopulmonary dysplasia (BPD) is a prevalent chronic lung disease in extremely preterm infants, characterized by arrested alveolarization and pulmonary vascular impairment. In neonatal mice and A549 cells, hyperoxia exposure significantly downregulated SIRT3 expression and PDH activity, resulting in severe mitochondrial structural and functional damage. Quantitative acetylome analysis revealed this deficiency leads to the hyperacetylation of PDHA1 at lysine 83. This modification inhibits PDH activity, forcing a pathogenic metabolic shift toward lactate accumulation and mitochondrial dysfunction. In vitro, a deacetylation-mimetic PDHA1-K83R mutant restored PDH activity and mitigated hyperoxia-induced mitochondrial injury.

Indexed as

Biochemical mechanismBiochemistryBiological sciencesHealth sciences

Identifiers

PMID42491861
PMCPMC13378344

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.