Evidence map›Paper›PMID 36896463›Full record

ArticlePharmaceutical biology2023

Tongmai Yangxin pill alleviates myocardial no-reflow by activating GPER to regulate HIF-1α signaling and downstream potassium channels.

Ting Chen, Yulong Zhang, Manyun Chen, Pu Yang, Yi Wang, Wei Zhang, Weihua Huang, Wei Zhang

Open access · goldFull text read
PubMed Full text at PMC Publisher
In one paragraph

Article in Pharmaceutical biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
1.5field-weighted citation impact, top 18% of its field
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

1 citing paper in PubMed, 6 citations in OpenAlex.

  1. Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
    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

8 authors at 2 institutions in 1 country.

Ting ChenKey Laboratory of Hunan Province for Integrated Traditional Chinese and Western Medicine on Prevention and Treatment of Cardio-Cerebral Diseases, Hunan University of Chinese Medicine, Changsha, China.
Yulong ZhangDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, People's Republic of China.
Manyun ChenDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, People's Republic of China.
Pu YangDepartment of General Surgery, Xiangya Hospital, Central South University, Changsha, People's Republic of China.
Yi WangInstitute of Traditional Chinese medicine, Tianjin University of Traditional Chinese medicine, Tianjin, People's Republic of China.
Wei ZhangKey Laboratory of Hunan Province for Integrated Traditional Chinese and Western Medicine on Prevention and Treatment of Cardio-Cerebral Diseases, Hunan University of Chinese Medicine, Changsha, China.
Weihua HuangDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, People's Republic of China.
Wei ZhangDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, People's Republic of China.
Central South University · CNTianjin University of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

contextThe Tongmai Yangxin pill (TMYX) has potential clinical effects on no-reflow (NR); however, the effective substances and mechanisms remain unclear.

objectiveThis study evaluates the cardioprotective effects and molecular mechanisms of TMYX against NR. MATERIALS AND

methodsWe used a myocardial NR rat model to confirm the effect and mechanism of action of TMYX in alleviating NR. Sprague-Dawley (SD) rats were divided into Control (Con), sham, NR, TMYX (4.0 g/kg), and sodium nitroprusside (SNP, 5.0 mg/kg), and received their treatments once a day for one week.

resultsTMYX (4.0 g/kg) showed therapeutic effects on NR by improving the cardiac structure and function, reducing NR, ischemic areas, and cardiomyocyte injury, and decreasing the expression of cardiac troponin I (cTnI). Moreover, the mechanism of TMYX predicted by network pharmacology is related to the HIF-1, NF-κB, and TNF signaling pathways.

conclusionsTMYX exerts its pharmacological effects in the treatment of NR

Indexed as

NF-kappa BPotassium ChannelsAnimalsDrugs, Chinese HerbalHypoxia-Inducible Factor 1, alpha SubunitIschemiaMyocytes, CardiacRatsRats, Sprague-DawleyReceptors, G-Protein-CoupledDrugs, Chinese HerbalGper1 protein, ratHif1a protein, ratHypoxia-Inducible Factor 1, alpha SubunitNF-kappa BPotassium ChannelsReceptors, G-Protein-CoupledCardioprotective effectscoronary microvasculaturemolecular mechanismsnetwork pharmacology

Identifiers

PMID36896463
PMCPMC10013430
OpenAlexW4323805725

What OpenQuestion holds

Textfull text, public
LicenceCC BY
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Read underepoch 390

Registered trials

None linked

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.