Evidence map›Paper›PMID 38812011›Full record

ArticleCardiovascular diabetology2024

Inhibition of Slc39a14/Slc39a8 reduce vascular calcification via alleviating iron overload induced ferroptosis in vascular smooth muscle cells.

Yierpani Aierken, Huqiang He, Runwen Li, Zipeng Lin, Tongjie Xu, Li Zhang, Ya Wu, Yong Liu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cardiovascular diabetology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing 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

21 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Iron Dysregulation and Vascular Diseases: A Contemporary Review.Journal of the American Heart Association · 2026
    Review
  7. Article
  8. Review
  9. Iron in Vascular Calcification: Pro-Calcific Agent or Protective Modulator?International journal of molecular sciences · 2025
    Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  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

8 authors.

Yierpani Aierken *Department of Vascular Surgery, The Affiliated Hospital, Southwest Medical University, No. 25, Taiping Street, Luzhou, 646000, Sichuan, China.
Huqiang He *Department of Vascular Surgery, The Affiliated Hospital, Southwest Medical University, No. 25, Taiping Street, Luzhou, 646000, Sichuan, China.
Runwen LiDepartment of Vascular Surgery, The Affiliated Hospital, Southwest Medical University, No. 25, Taiping Street, Luzhou, 646000, Sichuan, China.
Zipeng LinDepartment of Vascular Surgery, The Affiliated Hospital, Southwest Medical University, No. 25, Taiping Street, Luzhou, 646000, Sichuan, China.
Tongjie XuDepartment of Vascular Surgery, The Affiliated Hospital, Southwest Medical University, No. 25, Taiping Street, Luzhou, 646000, Sichuan, China.
Li ZhangDepartment of Vascular Surgery, The Affiliated Hospital, Southwest Medical University, No. 25, Taiping Street, Luzhou, 646000, Sichuan, China.
Ya WuDepartment of Vascular Surgery, The Affiliated Hospital, Southwest Medical University, No. 25, Taiping Street, Luzhou, 646000, Sichuan, China. yawu@swmu.du.cn.
Yong LiuDepartment of Vascular Surgery, The Affiliated Hospital, Southwest Medical University, No. 25, Taiping Street, Luzhou, 646000, Sichuan, China. lyong74@swmu.edu.cn.

Funding

National Natural Science Foundation of China 82200432the Foundation of Sichuan Provincial Medical Association S23010the Key Laboratory of Medical Electrophysiology (Southwest Medical University) KeyME-2022-08the Luzhou-Southwest Medical University cooperation project 2021LZXNYD-D11the Luzhou-Southwest Medical University cooperation project 2023LZXNYDJ043the Luzhou-Southwest Medical University cooperation project 2023LZXNYDT013the Natural Science Foundation of Sichuan Province of China 2022NSFSC1448
6 · The paper itself

Abstract

backgroundVascular calcification (VC) is an independent risk factor for cardiovascular diseases. Recently, ferroptosis has been recognised as a novel therapeutic target for cardiovascular diseases. Although an association between ferroptosis and vascular calcification has been reported, the role and mechanism of iron overload in vascular calcification are still poorly understood. Specifically, further in-depth research is required on whether metalloproteins SLC39a14 and SLC39a8 are involved in ferroptosis induced by iron overload.

methodsR language was employed for the differential analysis of the dataset, revealing the correlation between ferroptosis and calcification. The experimental approaches encompassed both in vitro and in vivo studies, incorporating the use of iron chelators and models of iron overload. Additionally, gain- and loss-of-function experiments were conducted to investigate iron's effects on vascular calcification comprehensively. Electron microscopy, immunofluorescence, western blotting, and real-time polymerase chain reaction were used to elucidate how Slc39a14 and Slc39a8 mediate iron overload and promote calcification.

resultsFerroptosis was observed in conjunction with vascular calcification (VC); the association was consistently confirmed by in vitro and in vivo studies. Our results showed a positive correlation between iron overload in VSMCs and calcification. Iron chelators are effective in reversing VC and iron overload exacerbates this process. The expression levels of the metal transport proteins Slc39a14 and Slc39a8 were significantly upregulated during calcification; the inhibition of their expression alleviated VC. Conversely, Slc39a14 overexpression exacerbates calcification and promotes intracellular iron accumulation in VSMCs.

conclusionsOur research demonstrates that iron overload occurs during VC, and that inhibition of Slc39a14 and Slc39a8 significantly relieves VC by intercepting iron overload-induced ferroptosis in VSMCs, providing new insights into the VC treatment.

Indexed as

Cation Transport ProteinsDisease Models, AnimalFerroptosisIron Chelating AgentsMice, Inbred C57BLMuscle, Smooth, VascularMyocytes, Smooth MuscleVascular CalcificationAnimalsHumansIronIron OverloadMaleSignal TransductionCation Transport ProteinsIronIron Chelating AgentsSLC39A14 protein, humanSLC39A14 protein, mouseSLC39A8 protein, humanFerroptosisIron overloadIron transportOxidative stressVascular calcification

Identifiers

PMID38812011
PMCPMC11138056

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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.