Evidence map›Paper›PMID 34376636›Full record

ReviewCell death & disease2021

Ferroptosis: the potential value target in atherosclerosis.

Siyu Ouyang, Jia You, Chenxi Zhi, Pin Li, Xiaoyan Lin, Xiaoqian Tan, Wentao Ma, Liang Li, Wei Xie

Open access · goldAbstract readReview
In one paragraph

Review in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
113citing papers in PubMed, 2 pooled it
17.0field-weighted citation impact, top 1% 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

113 citing papers in PubMed, 2 syntheses or guidelines pooled it, 172 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  5. Review
  6. Article
  7. Review
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  9. Distinct types of regulated cell death in atherosclerosis.Journal of pharmaceutical analysis · 2026
    Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Novel insights of ferroptosis in atherosclerosis progression.Frontiers in cell and developmental biology · 2026
    Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article

53 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Siyu OuyangClinical Anatomy & Reproductive Medicine Application Institute, University of South China, Hengyang, 421001, Hunan, China.
Jia YouClinical Anatomy & Reproductive Medicine Application Institute, University of South China, Hengyang, 421001, Hunan, China.
Chenxi ZhiClinical Anatomy & Reproductive Medicine Application Institute, University of South China, Hengyang, 421001, Hunan, China.
Pin LiClinical Anatomy & Reproductive Medicine Application Institute, University of South China, Hengyang, 421001, Hunan, China.
Xiaoyan LinInstitute of Cardiovascular Research, Key Laboratory for Atherosclerology of Hunan Province, Medical Research Center, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, University of South China, Hengyang, 421001, Hunan, China.
Xiaoqian TanClinical Anatomy & Reproductive Medicine Application Institute, University of South China, Hengyang, 421001, Hunan, China.
Wentao MaClinical Anatomy & Reproductive Medicine Application Institute, University of South China, Hengyang, 421001, Hunan, China.
Liang LiInstitute of Cardiovascular Research, Key Laboratory for Atherosclerology of Hunan Province, Medical Research Center, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, University of South China, Hengyang, 421001, Hunan, China. 26002860@qq.com.
Wei XieClinical Anatomy & Reproductive Medicine Application Institute, University of South China, Hengyang, 421001, Hunan, China. weixiehy@126.com.ORCID 0000-0003-0568-5304
University of South China · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81800386
6 · The paper itself

Abstract

In advanced atherosclerosis (AS), defective function-induced cell death leads to the formation of the characteristic necrotic core and vulnerable plaque. The forms and mechanisms of cell death in AS have recently been elucidated. Among them, ferroptosis, an iron-dependent form of necrosis that is characterized by oxidative damage to phospholipids, promotes AS by accelerating endothelial dysfunction in lipid peroxidation. Moreover, disordered intracellular iron causes damage to macrophages, vascular smooth muscle cells (VSMCs), vascular endothelial cells (VECs), and affects many risk factors or pathologic processes of AS such as disturbances in lipid peroxidation, oxidative stress, inflammation, and dyslipidemia. However, the mechanisms through which ferroptosis initiates the development and progression of AS have not been established. This review explains the possible correlations between AS and ferroptosis, and provides a reliable theoretical basis for future studies on its mechanism.

Indexed as

FerroptosisAnimalsAtherosclerosisHumansIronLipid PeroxidationModels, BiologicalReactive Oxygen SpeciesIronReactive Oxygen Species

Identifiers

PMID34376636
PMCPMC8355346
OpenAlexW3191708101

What OpenQuestion holds

Textmetadata
LicenceCC BY
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 OpenQuestion graph.