Evidence map›Paper›PMID 39261835›Full record

ArticleParticle and fibre toxicology2024

Microplastics caused embryonic growth retardation and placental dysfunction in pregnant mice by activating GRP78/IRE1α/JNK axis induced apoptosis and endoplasmic reticulum stress.

Jun Bai, Yuzeng Wang, Siwei Deng, Ying Yang, Sheng Chen, Zhenlong Wu

Abstract read
In one paragraph

Article in Particle and fibre toxicology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
–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

20 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Micro and Nanoplastics and Obstetric Outcomes in Humans and Animals: A Systematic Review.International journal of environmental research and public health · 2026
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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

6 authors.

Jun BaiState Key Laboratory of Animal Nutrition and Feeding, Department of Companion Animal Science, China Agricultural University, Beijing, China.
Yuzeng WangState Key Laboratory of Animal Nutrition and Feeding, Department of Companion Animal Science, China Agricultural University, Beijing, China.
Siwei DengState Key Laboratory of Animal Nutrition and Feeding, Department of Companion Animal Science, China Agricultural University, Beijing, China.
Ying YangState Key Laboratory of Animal Nutrition and Feeding, Department of Companion Animal Science, China Agricultural University, Beijing, China.
Sheng ChenState Key Lab of Chemical Biology and Drug Discovery, Department of Food Science and Nutrition, The Hong Kong Polytechnic University, Hom Hung, Kowloon, Hong Kong, China.
Zhenlong WuState Key Laboratory of Animal Nutrition and Feeding, Department of Companion Animal Science, China Agricultural University, Beijing, China. bio2046@hotmail.com.

Funding

National Natural Science Foundation of China 31625025
6 · The paper itself

Abstract

Microplastics (MPs), a brand-new class of worldwide environmental pollutant, have received a lot of attention. MPs are consumed by both humans and animals through water, food chain and other ways, which may cause potential health risks. However, the effects of MPs on embryonic development, especially placental function, and its related mechanisms still need to be further studied. We investigated the impact on fetal development and placental physiological function of pregnant mice by consecutive gavages of MPs at 0, 25, 50, 100 mg/kg body weight during gestational days (GDs 0-14). The results showed that continuous exposure to high concentrations of MP significantly reduced daily weight gain and impaired reproductive performance of pregnant mice. In addition, MPs could significantly induce oxidative stress and placental dysfunction in pregnant mice. On the other hand, MPs exposure significantly decreased placental barrier function and induced placental inflammation. Specifically, MPs treatment significantly reduced the expression of tight junction proteins in placentas, accompanied by inflammatory cell infiltration and increased mRNA levels of pro-inflammatory cytokines and chemokines in placentas. Finally, we found that MPs induced placental apoptosis and endoplasmic reticulum (ER) stress through the GRP78/IRE1α/JNK axis, leading to placental dysfunction and decreased reproductive performance in pregnant mice. We revealed for the first time that the effects of MPs on placental dysfunction in pregnant animals. Blocking the targets of MPs mediated ER stress will provide potential therapeutic ideas for the toxic effects of MPs on maternal pregnancy.

Indexed as

ApoptosisEndoplasmic Reticulum Chaperone BiPEndoplasmic Reticulum StressMicroplasticsPlacentaAnimalsFemaleFetal Growth RetardationHeat-Shock ProteinsMiceMice, Inbred ICROxidative StressPregnancyProtein Serine-Threonine KinasesEndoplasmic Reticulum Chaperone BiPHeat-Shock ProteinsHSPA5 protein, humanHspa5 protein, mouseMicroplasticsProtein Serine-Threonine KinasesDevelopmental toxicityEndoplasmic reticulum stressMAPK pathwayMicroplasticsPlacentaPregnant mice

Identifiers

PMID39261835
PMCPMC11389422

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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.