Evidence map›Paper›PMID 42474070›Full record

ArticleJournal of cellular and molecular medicine2026

Qiliqiangxin Improves Cardiac Glucose Metabolism After Myocardial Infarction Through a HIF-1α/MIF/AMPK Axis.

Zimu Wang, Zhonglei Xie, Hanqing Zhao, Chaofu Li, Yanyan Wang, Yu Song, Ya'nan Qu, Jingfeng Wang, Jingmin Zhou

Abstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

9 authors.

Zimu WangDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, Shanghai, China.
Zhonglei XieDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, Shanghai, China.
Hanqing ZhaoDepartment of Rehabilitation Medicine, Xuzhou Center Hospital, Jiangsu Province, China.ORCID 0009-0000-2847-3828
Chaofu LiBioengineering College of Chongqing University, Chongqing University Central Hospital (Chongqing Emergency Medical Center), Chongqing, China.ORCID 0000-0002-7100-5787
Yanyan WangDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, Shanghai, China.
Yu SongDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, Shanghai, China.
Ya'nan QuDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, Shanghai, China.
Jingfeng WangDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, Shanghai, China.
Jingmin ZhouDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, Shanghai, China.

Funding

General Program of Natural Science Foundation of Shanghai 24ZR1461400National Natural Science Foundation of China 81870177Shanghai Municipal Health and Family Planning Commission No. 2018JP002
6 · The paper itself

Abstract

Cardiac glucose metabolism is critically involved in the pathophysiology of myocardial infarction. This study investigated whether Qiliqiangxin (QL), a traditional Chinese medicine, improves myocardial glucose uptake and aerobic oxidation after myocardial infarction (MI) and explored the underlying mechanisms. QL treatment significantly increased LVEF, enhanced myocardial glucose uptake, reduced fibrosis, apoptosis, ROS production and elevated ATP generation along with activity of pyruvate dehydrogenase (PDH) and citrate synthase (CS). These effects were abolished by HIF-1α-shRNA transduction. QL also upregulated the expression of HIF-1α, MIF, p-AMPKα, GLUT-4, hexokinase 2 (HK2), PDH and CS, which were similarly attenuated by HIF-1α knockdown. In conclusion, our study demonstrated that QL enhances myocardial glucose uptake and aerobic oxidation in a murine model of post-MI heart failure. Genetic inhibition of HIF-1α reverses these beneficial effects, suggesting the involvement of the HIF-1α/MIF/AMPK signalling axis.

Indexed as

AMP-Activated Protein KinasesDrugs, Chinese HerbalGlucoseHypoxia-Inducible Factor 1, alpha SubunitMyocardial InfarctionMyocardiumAnimalsApoptosisMiceReactive Oxygen SpeciesSignal TransductionAMP-Activated Protein KinasesDrugs, Chinese HerbalGlucoseHypoxia-Inducible Factor 1, alpha SubunitqiliqiangxinReactive Oxygen Speciesglucose metabolismmyocardial infarctionQiliqiangxin (QL)

Identifiers

PMID42474070
PMCPMC13383748

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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.