Evidence map›Paper›PMID 39744431›Full record

ArticleInternational journal of biological sciences2025

Ganglioside GA2-mediated caspase-11 activation drives macrophage pyroptosis aggravating intimal hyperplasia after arterial injury.

Yunmin Shi, Tian He, Hong Liu, Xiaodong Li, Zhengxin Li, Qing Wen, Zhaohui Dai, Xuejing Sun, Qian Tan, Wenjing Yang and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of biological sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Review
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  5. Review
  6. 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

16 authors.

Yunmin ShiDepartment of Cardiology, Third Xiangya Hospital, Central South University, Changsha, 410013, Hunan, China.
Tian HeDepartment of Cardiology, Third Xiangya Hospital, Central South University, Changsha, 410013, Hunan, China.
Hong LiuDepartment of Cardiology, Third Xiangya Hospital, Central South University, Changsha, 410013, Hunan, China.
Xiaodong LiDepartment of Cardiovascular Medicine, Department of Hypertension, Ruijin Hospital and State Key Laboratory of Medical Genomics, Shanghai Key Laboratory of Hypertension, Shanghai Institute of Hypertension, Shanghai Jiao Tong University School of Medicine, 200020, China.
Zhengxin LiDepartment of Cardiology, Third Xiangya Hospital, Central South University, Changsha, 410013, Hunan, China.
Qing WenDepartment of Cardiology, Third Xiangya Hospital, Central South University, Changsha, 410013, Hunan, China.
Zhaohui DaiDepartment of Cardiology of the Fourth Hospital of Changsha, Changsha Hospital of Hunan Normal University, Changsha, 410006, Hunan, China.
Xuejing SunDepartment of Cardiology, Third Xiangya Hospital, Central South University, Changsha, 410013, Hunan, China.
Qian TanDepartment of Cardiology, Third Xiangya Hospital, Central South University, Changsha, 410013, Hunan, China.
Wenjing YangDepartment of Cardiology, Third Xiangya Hospital, Central South University, Changsha, 410013, Hunan, China.
Youxiang JiangDepartment of Cardiology, Third Xiangya Hospital, Central South University, Changsha, 410013, Hunan, China.
Yuanyuan LiuDepartment of Cardiology, Third Xiangya Hospital, Central South University, Changsha, 410013, Hunan, China.
Hong YuanDepartment of Cardiology, Third Xiangya Hospital, Central South University, Changsha, 410013, Hunan, China.
Fang LeiMedical Science Research Center, Zhongnan Hospital of Wuhan University, Wuhan, 430000, Hubei, China.
Yang YiDepartment of Cardiovascular Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200020, Shanghai, China.
Jingjing CaiDepartment of Cardiology, Third Xiangya Hospital, Central South University, Changsha, 410013, Hunan, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intimal hyperplasia (IH) remains a significant clinical problem, causing vascular intervention failure. This study aimed to elucidate whether gangliosides GA2 accumulated in atherosclerotic mouse aortae and plasma promote the development of IH. We identified that GA2 was remarkably accumulated in both artery and plasma of atherosclerotic patients and mice. Injected GA2 exacerbated IH and mainly co-stained with macrophages after mouse carotid arterial injury model. Intracellular GA2 induced pyroptosis accompanying the IL-1α release, which was blocked by caspase-11 knockout. Mechanistically, GA2 directly activated caspase-4 as a new ligand. And then, activated caspase-4/11 combined and cleaved BID, promoting the cytochrome C release to cytoplasm, which derived gasdermin E-medicated pyroptosis through activation of caspase-9-caspase-3 pathway. Mice transplanted with caspase-11 deficient bone marrow or mice with caspase-11 knockdown in macrophages exhibited an improvement of the IH aggravated by GA2. These findings suggest GA2-mediated caspase-4/11 activation drives macrophage pyroptosis, contributing to IH. Our results provide a potential diagnostic and therapeutic target in IH.

Indexed as

Carotid Artery InjuriesCaspases, InitiatorGangliosidesMacrophagesPyroptosisAnimalsApolipoproteins EBone MarrowCell LineEnzyme ActivationFemaleHumansHyperplasiaMaleMice, Inbred C57BLMice, KnockoutApoe protein, mouseApolipoproteins ECasp4 protein, mouseCaspases, Initiatorganglio-N-triaosylceramideGangliosides

Identifiers

PMID39744431
PMCPMC11667815

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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.