Evidence map›Paper›PMID 42331842›Full record

ArticleNature communications2026

AOC1 regulates labor initiation through spermidine-induced autophagy of placental trophoblast cells via EIF5A hypusination.

Huaiyan Chen, Peihua Long, Zhe Wang, Ruoheng Du, Chagui Zheng, Zhuo Li, Yihuan Xu, Qiaozhen Peng, Xuesong Sui, Yanyu Sui and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 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

13 authors.

Huaiyan Chen *Department of Physiology, Naval Medical University, Shanghai, China.
Peihua Long *Department of Physiology, Naval Medical University, Shanghai, China.ORCID http://orcid.org/0009-0002-5562-7890
Zhe Wang *Department of Physiology, Naval Medical University, Shanghai, China.
Ruoheng Du *Department of Physiology, Naval Medical University, Shanghai, China.
Chagui ZhengDepartment of Physiology, Naval Medical University, Shanghai, China.
Zhuo LiDepartment of Physiology, Naval Medical University, Shanghai, China.
Yihuan XuDepartment of Physiology, Naval Medical University, Shanghai, China.
Qiaozhen PengDepartment of Gynecology and Obstetrics, Xiangya Hospital, Central South University, Changsha, China.
Xuesong SuiDepartment of Physiology, Naval Medical University, Shanghai, China.
Yanyu SuiDepartment of Physiology, Naval Medical University, Shanghai, China.
Xiang JiangDepartment of Gynecology and Obstetrics, Shanghai First Maternity and Infant Hospital, Tongji University, Shanghai, China.
Qin LiDepartment of Gynecology and Obstetrics, Shanghai Changhai Hospital, Naval Medical University, Shanghai, China.
Lu GaoDepartment of Physiology, Naval Medical University, Shanghai, China. roadgao@163.com.ORCID http://orcid.org/0000-0003-2170-2645

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parturition depends on precise communication between the mother and fetus. While fetal lung signals are known to help initiate labor, the role of the placenta has remained unclear. Here we show that in steroid receptor coactivator (Src)-1 and -2 double-knockout mice, reduced placental amine oxidase, copper-containing 1 (Aoc1) leads to increased spermidine levels. In trophoblast cells, spermidine induces autophagy via hypusination of eukaryotic translation initiation factor 5 A (EIF5A), reducing estrogen and prostaglandin production. Estrogen reciprocally increases Aoc1 expression via estrogen receptor-α (ERα) in concert with SRC-1/2, forming a feedback loop maintaining placental autophagy homeostasis. AOC1 levels are elevated in preterm labor placentas from both mice and humans. Placenta-specific Aoc1 knockout dramatically delays labor by increasing trophoblast autophagy. Importantly, spermidine supplementation rescues inflammation-induced preterm labor in mice. Our findings reveal that placental AOC1-spermidine-EIF5A-autophagy axis is essential for parturition timing and offer a potential therapeutic strategy for preterm birth.

Indexed as

AutophagyLabor, ObstetricOxidoreductases Acting on CH-NH Group DonorsPeptide Initiation FactorsPlacentaRNA-Binding ProteinsSpermidineTrophoblastsAnimalsEstrogen Receptor alphaEukaryotic Translation Initiation Factor 5AFemaleHumansMiceMice, KnockoutObstetric Labor, PrematureEstrogen Receptor alphaEukaryotic Translation Initiation Factor 5AOxidoreductases Acting on CH-NH Group DonorsPeptide Initiation FactorsRNA-Binding ProteinsSpermidine

Identifiers

PMID42331842
PMCPMC13438134

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Registered trials

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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.