Evidence map›Paper›PMID 42490037›Full record

ArticleCardiovascular toxicology2026

Tnxb Alleviates Myocardial Ischemia-Reperfusion Injury Through Facilitating Akt-Dependent Endothelial Cell Survival and Angiogenesis in Mice.

Haohao Hao, Xiaolin Zi, Yunhao Jiang, Jiawen Li

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Article in Cardiovascular toxicology, 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

4 authors.

Haohao HaoDepartment of Medical Ultrasound, The Fourth Affiliated Hospital of Harbin Medical University, Harbin, 150001, Heilongjiang, P.R. China.
Xiaolin ZiDepartment of Oncology, The Fourth Affiliated Hospital of Harbin Medical University, Harbin, 150001, Heilongjiang, P.R. China.
Yunhao JiangDepartment of Intensive Care Medicine, Daqing People's Hospital, Daqing, 246004, Heilongjiang, P.R. China.
Jiawen LiDepartment of Cardiology, The Fourth Affiliated Hospital of Harbin Medical University, No. 37, Yiyuan Street, Nangang District, Harbin, 150001, Heilongjiang, P.R. China. 602178@hrbmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tenascin-X (Tnxb) is a large extracellular matrix protein that has been associated with atherosclerosis. The objective of this study was to investigate the effect of Tnxb and its contribution to recovery after myocardial ischemia/reperfusion (I/R) injury. Tnxb expression was reduced in ECs of mice with ligation of the left anterior descending. Conditional Tnxb overexpression using adeno-associated viruses promoted Akt phosphorylation and mitigated myocardial injury and cardiac dysfunction in mice with myocardial I/R. Furthermore, overexpression of Tnxb alleviated apoptosis and enhanced angiogenesis in vivo and in vitro. Krueppel-like factor 4 (Klf4) recruited SWItch/sucrose nonfermentable (SWI/SNF) to the distal enhancer of Tnxb to transcriptionally activate Tnxb, thereby promoting Akt phosphorylation. The mitigating effect of Klf4 overexpression on I/R-induced endothelial apoptosis and angiogenic dysfunction was dependent on Tnxb activation, since Tnxb knockdown reversed the effects of Klf4 overexpression on myocardial I/R injury. In summary, we show that Klf4 recruits SWI/SNF to the distal enhancer of Tnxb to transcriptionally activate Tnxb, which promotes Akt phosphorylation and alleviates myocardial I/R-induced endothelial apoptosis and angiogenic dysfunction. Lastly, Tnxb was identified as a potential therapeutic target in EC injuries induced by myocardial I/R.

Indexed as

Endothelial CellsMyocardial Reperfusion InjuryNeovascularization, PhysiologicProto-Oncogene Proteins c-aktAnimalsApoptosisCells, CulturedCell SurvivalDisease Models, AnimalHumansKruppel-Like Factor 4Kruppel-Like Transcription FactorsMaleMiceMice, Inbred C57BLPhosphorylationKlf4 protein, mouseKruppel-Like Factor 4Kruppel-Like Transcription FactorsProto-Oncogene Proteins c-aktEndothelial cellsEnhancerKlf4Myocardial ischemia/reperfusionTnxb

Identifiers

PMID42490037

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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.