Evidence map›Paper›PMID 40259193›Full record

ArticleJournal of cardiovascular translational research2025

Inhibition of VSMC Ferroptosis Mitigates Pathological Vascular Remodeling: A Novel Therapeutic Strategy for Abdominal Aortic Aneurysm.

Yating Zhou, Yanyu Chen, Yuting Cui, Ni Gan, Qiong Xiang, Man Li, Wen Zeng, Xi-Long Zheng, Xiaoyan Dai, Juan Peng and 1 more

Abstract read
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In one paragraph

Article in Journal of cardiovascular translational research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. 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

11 authors.

Yating ZhouInstitute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan Province, Hunan International Scientific and Technological Cooperation Base of Arteriosclerotic Disease, School of Basic Medical Sciences, Hengyang Medical School, University of South China, Hengyang, 421001, China.
Yanyu ChenInstitute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan Province, Hunan International Scientific and Technological Cooperation Base of Arteriosclerotic Disease, School of Basic Medical Sciences, Hengyang Medical School, University of South China, Hengyang, 421001, China.
Yuting CuiInstitute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan Province, Hunan International Scientific and Technological Cooperation Base of Arteriosclerotic Disease, School of Basic Medical Sciences, Hengyang Medical School, University of South China, Hengyang, 421001, China.
Ni GanInstitute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan Province, Hunan International Scientific and Technological Cooperation Base of Arteriosclerotic Disease, School of Basic Medical Sciences, Hengyang Medical School, University of South China, Hengyang, 421001, China.
Qiong XiangInstitute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan Province, Hunan International Scientific and Technological Cooperation Base of Arteriosclerotic Disease, School of Basic Medical Sciences, Hengyang Medical School, University of South China, Hengyang, 421001, China.
Man LiInstitute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan Province, Hunan International Scientific and Technological Cooperation Base of Arteriosclerotic Disease, School of Basic Medical Sciences, Hengyang Medical School, University of South China, Hengyang, 421001, China.
Wen ZengShaoyang Branch of Key Laboratory for Arteriosclerology of Hunan Province, The Central Hospital of Shaoyang, Shaoyang, 421001, China.
Xi-Long ZhengDepartments of Biochemistry & Molecular Biology and Physiology & Pharmacology, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada.
Xiaoyan DaiClinical Research Center, the Second Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, 421002, China. xdai@usc.edu.cn.
Juan PengInstitute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan Province, Hunan International Scientific and Technological Cooperation Base of Arteriosclerotic Disease, School of Basic Medical Sciences, Hengyang Medical School, University of South China, Hengyang, 421001, China. pengjuan98@sina.com.
Zhihan TangInstitute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan Province, Hunan International Scientific and Technological Cooperation Base of Arteriosclerotic Disease, School of Basic Medical Sciences, Hengyang Medical School, University of South China, Hengyang, 421001, China. tangzhihan98@163.com.ORCID 0000-0001-8191-7950

Funding

Guidance Program of Health Commission of Hunan Province 20201905Hunan Provincial Health High-Level Talent Scientific Research Project R2023046the Natural Science Foundation of Hunan Province 2025JJ90128
6 · The paper itself

Abstract

Ferroptosis plays a key role in abdominal aortic aneurysm (AAA) development. This study explores whether and how ferroptosis regulates AAA progression. Ferroptosis was confirmed in human AAA tissue. In vitro experiments with primary mouse vascular smooth muscle cells (VSMCs) and abdominal aortic rings revealed that angiotensin II (Ang II) triggered ferroptosis in VSMCs. Ferrostatin-1 (Fer-1), a potent ferroptosis inhibitor, effectively suppressed this effect. Additionally, the ferroptosis inducer erastin and Ang II can both promoted pathological remodeling of abdominal aortic rings, but Fer-1 significantly suppressed these effects. In AAA mouse model, Fer-1 treatment reduced AAA formation. Mechanistically, RNA-sequencing analysis revealed that Fer-1 regulates VSMC contractile function, suppresses inflammation, and mitigates extracellular matrix remodeling. These findings highlight the critical role of VSMC ferroptosis in AAA pathogenesis and demonstrate that ferroptosis inhibition effectively reduces pathological vascular remodeling, making it a promising therapeutic strategy for preventing AAA.

Indexed as

Aorta, AbdominalAortic Aneurysm, AbdominalCyclohexylaminesFerroptosisMuscle, Smooth, VascularMyocytes, Smooth MusclePhenylenediaminesVascular RemodelingAngiotensin IIAnimalsCells, CulturedDisease Models, AnimalHumansMaleMiceMice, Inbred C57BLAngiotensin IICyclohexylaminesferrostatin-1PhenylenediaminesAbdominal aortic aneurysmFerroptosisFerrostatin-1Pathological vascular remodelingVascular smooth muscle cell

Identifiers

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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.