Evidence map›Paper›PMID 41814330›Full record

ArticleJournal of nanobiotechnology2026

PET-microplastics trigger endothelial glycocalyx loss via ER stress and ROS unleashing IL-1β-driven SMC switching and early aortic structural impairment.

Weixue Huo, Jin Qu, Sen Wang, Mengwei He, Zhaoxiang Zeng, Deping Kong, Lushun Yuan, Rui Feng

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of nanobiotechnology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

8 authors.

Weixue Huo *Department of Vascular Surgery, Intervention Center, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200080, People's Republic of China.
Jin Qu *Department of Vascular Surgery, Intervention Center, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200080, People's Republic of China.
Sen Wang *Department of Vascular Surgery, Intervention Center, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200080, People's Republic of China.
Mengwei HeDepartment of Vascular Surgery, Intervention Center, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200080, People's Republic of China.
Zhaoxiang ZengDepartment of Vascular Surgery, Intervention Center, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200080, People's Republic of China.
Deping KongPrecision Research Center for Refractory Diseases, Institute for Clinical Research, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200080, People's Republic of China.
Lushun YuanDepartment of Vascular Surgery, Intervention Center, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200080, People's Republic of China. yuanlushun@whu.edu.cn.
Rui FengDepartment of Vascular Surgery, Intervention Center, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200080, People's Republic of China. rui.feng@shgh.cn.

Funding

Joint Research Project for Emerging Frontier Technologies of Shanghai Shenkang Hospital Development Center SHDC12022107National Natural Science Foundation of China 82270505National Natural Science Foundation of China 82400835Shanghai Pujiang Programme 24PJD090
6 · The paper itself

Abstract

Polyethylene terephthalate microplastics (PET-MPs), a major microplastics component identified in human vasculature, pose emerging environmental health risks. This study systemically profiled MPs in human aortic tissues and investigated the mechanisms underlying PET-MPs-induced aortic injury in vivo and in vitro. Chronic oral exposure of Sprague-Dawley rats to PET-MPs resulted in endothelial glycocalyx loss and structural impairment of aortic elastic fibers. Transcriptomic and proteomic analyses elucidated that PET-MPs triggered endoplasmic reticulum stress and reactive oxygen species generation, initiating glycocalyx loss and inflammatory activation. This response further pinpointed interleukin-1β (IL-1β) as a pivotal mediator inducing smooth muscle cell phenotypic switching. Crucially, restoration of the glycocalyx using sulodexide mitigated endothelial dysfunction and downstream smooth muscle cells phenotypic switching. These findings establish endothelial glycocalyx degradation via endoplasmic reticulum stress-reactive oxygen species as a novel mechanism for PET-MPs-induced vascular injury and highlight glycocalyx protection as a potential strategy against environmental microplastic hazards.

Indexed as

AortaEndoplasmic Reticulum StressGlycocalyxInterleukin-1betaMicroplasticsMyocytes, Smooth MusclePolyethylene TerephthalatesReactive Oxygen SpeciesAnimalsHumansMaleRatsRats, Sprague-DawleyInterleukin-1betaMicroplasticsPolyethylene TerephthalatesReactive Oxygen SpeciesAortic structural impairmentEndoplasmic reticulum stress-reactive oxygen species axisEndothelial glycocalyxMicroplasticsPolyethylene terephthalate

Identifiers

PMID41814330
PMCPMC13094091

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

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 Socratic graph.