Evidence map›Paper›PMID 39123142›Full record

ArticleBMC cardiovascular disorders2024

Isoliquiritigenin attenuates myocardial ischemia reperfusion through autophagy activation mediated by AMPK/mTOR/ULK1 signaling.

Liying Shen, Yingwei Zhu, Zhenfeng Chen, Feng Shen, Weiwei Yu, Li Zhang

Abstract read
In one paragraph

Article in BMC cardiovascular disorders, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. Signaling Pathways and Therapeutic Approaches in Post-Myocardial Infarction Fibrosis.Medical science monitor : international medical journal of experimental and clinical research · 2025
    Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Colchicine prevents perioperative myocardial injury in cardiac surgery by inhibiting the formation of neutrophil extracellular traps: evidence from rat models.European journal of cardio-thoracic surgery : official journal of the European Association for Cardio-thoracic Surgery · 2024
    Article
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

6 authors.

Liying ShenDepartment of Cardiology, Huzhou Central Hospital, No. 1558, Sanhuan North Road, Wuxing District, Huzhou, 313000, Zhejiang, China.
Yingwei ZhuDepartment of Cardiology, Huzhou Central Hospital, No. 1558, Sanhuan North Road, Wuxing District, Huzhou, 313000, Zhejiang, China.
Zhenfeng ChenDepartment of Cardiology, Huzhou Central Hospital, No. 1558, Sanhuan North Road, Wuxing District, Huzhou, 313000, Zhejiang, China.
Feng ShenDepartment of Cardiology, Huzhou Central Hospital, No. 1558, Sanhuan North Road, Wuxing District, Huzhou, 313000, Zhejiang, China.
Weiwei YuDepartment of Cardiology, Huzhou Central Hospital, No. 1558, Sanhuan North Road, Wuxing District, Huzhou, 313000, Zhejiang, China.
Li ZhangDepartment of Cardiology, Huzhou Central Hospital, No. 1558, Sanhuan North Road, Wuxing District, Huzhou, 313000, Zhejiang, China. zhanglinbu2010@163.com.

Funding

Huzhou Cardiovascular and Cerebrovascular Disease Discipline Group XKQ-HT-202102APublic Technology Applied Research Program of Huzhou City 2023GY10
6 · The paper itself

Abstract

backgroundIschemia reperfusion (IR) causes impaired myocardial function, and autophagy activation ameliorates myocardial IR injury. Isoliquiritigenin (ISO) has been found to protect myocardial tissues via AMPK, with exerting anti-tumor property through autophagy activation. This study aims to investigate ISO capacity to attenuate myocardial IR through autophagy activation mediated by AMPK/mTOR/ULK1 signaling.

methodsISO effects were explored by SD rats and H9c2 cells. IR rats and IR-induced H9c2 cell models were established by ligating left anterior descending (LAD) coronary artery and hypoxia/re-oxygenation, respectively, followed by low, medium and high dosages of ISO intervention (Rats: 10, 20, and 40 mg/kg; H9c2 cells: 1, 10, and 100 μmol/L). Myocardial tissue injury in rats was assessed by myocardial function-related index, HE staining, Masson trichrome staining, TTC staining, and ELISA. Autophagy of H9c2 cells was detected by transmission electron microscopy (TEM) and immunofluorescence. Autophagy-related and AMPK/mTOR/ULK1 pathway-related protein expressions were detected with western blot.

resultsISO treatment caused myocardial function improvement, and inhibition of myocardial inflammatory infiltration, fibrosis, infarct area, oxidative stress, CK-MB, cTnI, and cTnT expression in IR rats. In IR-modeled H9c2 cells, ISO treatment lowered apoptosis rate and activated autophagy and LC3 fluorescence expression. In vivo and in vitro, ISO intervention exhibited enhanced Beclin1, LC3II/LC3I, and p-AMPK/AMPK levels, whereas inhibited P62, p-mTOR/mTOR and p-ULK1(S757)/ULK1 protein expression, activating autophagy and protecting myocardial tissues from IR injury.

conclusionISO treatment may induce autophagy by regulating AMPK/mTOR/ULK1 signaling, thereby improving myocardial IR injury, as a potential candidate for treatment of myocardial IR injury.

Indexed as

AMP-Activated Protein KinasesAutophagyAutophagy-Related Protein-1 HomologChalconesMyocardial Reperfusion InjuryMyocytes, CardiacRats, Sprague-DawleySignal TransductionTOR Serine-Threonine KinasesAnimalsApoptosisCell LineDisease Models, AnimalFibrosisMaleMyocardial InfarctionAMP-Activated Protein KinasesAutophagy-Related Protein-1 HomologChalconesisoliquiritigeninmTOR protein, ratTOR Serine-Threonine KinasesULK1 protein, ratAMPK/mTOR/ULK1AutophagyIschemia reperfusion injuryIsoliquiritigenin

Identifiers

PMID39123142
PMCPMC11311884

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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 OpenQuestion graph.