Evidence map›Paper›PMID 36192693›Full record

ArticleMolecular medicine (Cambridge, Mass.)2022

Induction of ferroptosis promotes vascular smooth muscle cell phenotypic switching and aggravates neointimal hyperplasia in mice.

Shunchi Zhang, Yanrou Bei, Yueling Huang, Yimin Huang, Lianjie Hou, Xi-Long Zheng, Yiming Xu, Shaoguo Wu, Xiaoyan Dai

Open access · goldAbstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
5.3field-weighted citation impact, top 3% of its field
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

27 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
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  9. Novel insights of ferroptosis in atherosclerosis progression.Frontiers in cell and developmental biology · 2026
    Review
  10. Review
  11. Article
  12. [Role of the TGFZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025
    Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Exosomes in arteriovenous fistula stenosis.Frontiers in cell and developmental biology · 2025
    Review
  19. Review
  20. 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

9 authors at 4 institutions in 2 countries.

Shunchi Zhang *Department of Clinical Laboratory, Guangzhou Twelfth People's Hospital, Guangzhou Municipal and Guangdong Provincial Key Laboratory of Molecular Target & Clinical Pharmacology, the NMPA and State Key Laboratory of Respiratory Disease, School of Pharmaceutical Sciences, Guangzhou Medical University, Guangzhou, 511436, Guangdong, China.
Yanrou Bei *Laboratory Medicine Center, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, Guangdong, China.
Yueling HuangExperimental Animal Center, Guangzhou Medical University, Guangzhou, 511436, Guangdong, China.
Yimin HuangDepartment of Clinical Laboratory, Guangzhou Twelfth People's Hospital, Guangzhou Municipal and Guangdong Provincial Key Laboratory of Molecular Target & Clinical Pharmacology, the NMPA and State Key Laboratory of Respiratory Disease, School of Pharmaceutical Sciences, Guangzhou Medical University, Guangzhou, 511436, Guangdong, China.
Lianjie HouThe Sixth Affiliated Hospital of Guangzhou Medical University, Qingyuan City People's Hospital, Qingyuan, 511518, Guangdong, China.
Xi-Long ZhengDepartment of Biochemistry & Molecular Biology, Cumming School of Medicine, University of Calgary, Calgary, AB, T2N 4Z6, Canada.
Yiming XuSchool of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, 511436, Guangdong, China.
Shaoguo WuDepartment of Clinical Laboratory, Guangzhou Twelfth People's Hospital, Guangzhou Municipal and Guangdong Provincial Key Laboratory of Molecular Target & Clinical Pharmacology, the NMPA and State Key Laboratory of Respiratory Disease, School of Pharmaceutical Sciences, Guangzhou Medical University, Guangzhou, 511436, Guangdong, China. wsg0930@163.com.
Xiaoyan DaiDepartment of Clinical Laboratory, Guangzhou Twelfth People's Hospital, Guangzhou Municipal and Guangdong Provincial Key Laboratory of Molecular Target & Clinical Pharmacology, the NMPA and State Key Laboratory of Respiratory Disease, School of Pharmaceutical Sciences, Guangzhou Medical University, Guangzhou, 511436, Guangdong, China. xdai@gzhmu.edu.cn.ORCID 0000-0001-5695-6384
State Key Laboratory of Respiratory Disease · CNGuangzhou Medical University · CNNanfang Hospital · CNUniversity of Calgary · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundStent implantation-induced neointima formation is a dominant culprit in coronary artery disease treatment failure after percutaneous coronary intervention. Ferroptosis, an iron-dependent regulated cell death, has been associated with various cardiovascular diseases. However, the effect of ferroptosis on neointima formation remains unclear.

methodsThe mouse common right carotid arteries were ligated for 16 or 30 days, and ligated tissues were collected for further analyses. Primary rat vascular smooth muscle cells (VSMCs) were isolated from the media of aortas of Sprague-Dawley (SD) rats and used for in vitro cell culture experiments.

resultsFerroptosis was positively associated with neointima formation. In vivo, RAS-selective lethal 3 (RSL3), a ferroptosis activator, aggravated carotid artery ligation-induced neointima formation and promoted VSMC phenotypic conversion. In contrast, a ferroptosis inhibitor, ferrostatin-1 (Fer-1), showed the opposite effects in mice. In vitro, RSL3 promoted rat VSMC phenotypic switching from a contractile to a synthetic phenotype, evidenced by increased contractile markers (smooth muscle myosin heavy chain and calponin 1), and decreased synthetic marker osteopontin. The induction of ferroptosis by RSL3 was confirmed by the increased expression level of ferroptosis-associated gene prostaglandin-endoperoxide synthase 2 (Ptgs2). The effect of RSL3 on rat VSMC phenotypic switching was abolished by Fer-1. Moreover, N-acetyl-L-cysteine (NAC), the reactive oxygen species inhibitor, counteracted the effect of RSL3 on the phenotypic conversion of rat VSMCs.

conclusionsFerroptosis induces VSMC phenotypic switching and accelerates ligation-induced neointimal hyperplasia in mice. Our findings suggest inhibition of ferroptosis as an attractive strategy for limiting vascular restenosis.

Indexed as

FerroptosisNeointimaAcetylcysteineAnimalsCell MovementCell ProliferationCells, CulturedCyclooxygenase 2Disease Models, AnimalHyperplasiaIronMiceMuscle, Smooth, VascularMyocytes, Smooth MuscleOsteopontinPhenotypeAcetylcysteineCyclooxygenase 2IronOsteopontinReactive Oxygen SpeciesSmooth Muscle MyosinsFerroptosisNeointimal hyperplasiaPhenotypic switchingROSVascular smooth muscle cells

Identifiers

PMID36192693
PMCPMC9528136
OpenAlexW4300817389

What OpenQuestion holds

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LicenceCC BY
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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.