Evidence map›Paper›PMID 41579229›Full record

ArticleCardiovascular drugs and therapy2026

High Mobility Group Protein B1 Mediates the Role of the Neutrophil Extracellular Traps in the Progression of Acute Myocardial Infarction.

Jing He, Landi Wang, Chen Xu, Jingyi Liu, Yuchao Wang, Jing Han, Jianhong Zhang, Dayong Li, Huanming Li, Yong Liu and 1 more

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Article in Cardiovascular drugs and therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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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

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

11 authors.

Jing He *Department of Cardiology, Tianjin Fourth Central Hospital, No.3, Zhongshan Road, Hebei District, Tianjin, 300140, China.
Landi Wang *School of Medicine, Tianjin University, Tianjin, China.
Chen Xu *Department of Clinical Laboratory, Tianjin Fourth Central Hospital, Tianjin, China.
Jingyi LiuSchool of Medicine, Tianjin University, Tianjin, China.
Yuchao WangGraduate School of Tianjin Medical University, Tianjin, China.
Jing HanSchool of Medicine, Tianjin University, Tianjin, China.
Jianhong ZhangPharmacy Department, Tianjin Fourth Central Hospital, No.3, Zhongshan Road, Hebei District, Tianjin, China.
Dayong LiGeneral surgery department, NHC Key Laboratory of Hormones and Development, Tianjin Key Laboratory of Metabolic Diseases, Tianjin Institute of Endocrinology, Chu Hsien-I Memorial Hospital, Tianjin Medical University, Tianjin, China.
Huanming LiDepartment of Cardiology, Tianjin Fourth Central Hospital, No.3, Zhongshan Road, Hebei District, Tianjin, 300140, China. 270129620@qq.com.
Yong LiuDepartment of Cardiology, Tianjin Fourth Central Hospital, No.3, Zhongshan Road, Hebei District, Tianjin, 300140, China. 13820788667@163.com.
Xuan LiuPharmacy Department, Tianjin Fourth Central Hospital, No.3, Zhongshan Road, Hebei District, Tianjin, China. cmdlx2022@126.com.

Funding

Atherosclerotic Cardiovascular Disease Prevention and Treatment Research Project of Beijing Jiekai Cardiovascular Health Foundation Project No. 2022-091Beijing Medical Award Foundation YXJL-2022-0734-0401Tianjin Fourth Central Hospital 2021 Outstanding Young Talents Key Training Object Training No.tjdszxyy20210006Tianjin Fourth Central Hospital 2021 Outstanding Young Talents Key Training Object Training tjdszxyy20210024
6 · The paper itself

Abstract

backgroundNeutrophil extracellular traps (NETs) play a crucial role in the pathogenesis of acute myocardial infarction (AMI), but the role of high-mobility group box 1 (HMGB1), a key target of the cell migration family, remains unclear.

methodsThis study investigated the HMGB1-CXCR4/CXCL12 -NETs pathway in ST-segment elevation myocardial infarction (STEMI) patients and a murine myocardial infarction (MI) model, with a focus on mechanisms associated with injury and aging.

resultsPeripheral blood analysis in 29 STEMI patients revealed elevated HMGB1 and myeloperoxidase (MPO) levels compared to controls. In C57BL/6J mice subjected to permanent left anterior descending (LAD) ligation, the CXCR4/CXCL12 axis was significantly upregulated in infarcted hearts, correlating with impaired ventricular function. Deoxyribonuclease (DNase) I or glycyrrhizic acid (a HMGB1 inhibitor) attenuated NETs formation and CXCR4/CXCL12 activation. Histological, echocardiographic, and transcriptomic analyses revealed that HMGB1 promotes NETs formation, exacerbating cardiac inflammation and fibrosis. Flow cytometry of murine blood demonstrated altered CD62L/CD11b expression, suggesting age-like immunophenotypic shifts in post-MI inflammation.

conclusionThese findings delineate a pivotal HMGB1-CXCR4/CXCL12-NETs axis in AMI pathology, driving cardiac injury through inflammation and fibrosis, with implications for cellular aging/senescence. Targeting this pathway presents a promising therapeutic strategy for mitigating ischemia-related damage.

Indexed as

Extracellular TrapsHMGB1 ProteinMyocardial InfarctionMyocardiumNeutrophilsAgedAnimalsCase-Control StudiesChemokine CXCL12Disease Models, AnimalDisease ProgressionFemaleFibrosisHumansMaleMice, Inbred C57BLChemokine CXCL12Cxcl12 protein, mouseCXCR4 protein, mouseHMGB1 ProteinHMGB1 protein, humanHMGB1 protein, mouseMPO protein, humanPeroxidaseReceptors, CXCR4Acute myocardial infarction“aged” neutrophilsHigh-mobility group box 1Neutrophil extracellular traps

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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 Socratic graph.