Evidence map›Paper›PMID 39206261›Full record

ArticleFrontiers in pharmacology2024

Puerarin attenuates myocardial ischemic injury and endoplasmic reticulum stress by upregulating the Mzb1 signal pathway.

Jiaojiao Xue, Haolin Ren, Qi Zhang, Jing Gu, Qian Xu, Jiaxi Sun, Lu Zhang, Ming-Sheng Zhou

Abstract read
In one paragraph

Article in Frontiers in pharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

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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.

Jiaojiao Xue *Science and Experiment Research Center, Shenyang Medical College, Shenyang, China.
Haolin Ren *Department of Radiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Qi ZhangScience and Experiment Research Center, Shenyang Medical College, Shenyang, China.
Jing GuScience and Experiment Research Center, Shenyang Medical College, Shenyang, China.
Qian XuScience and Experiment Research Center, Shenyang Medical College, Shenyang, China.
Jiaxi SunScience and Experiment Research Center, Shenyang Medical College, Shenyang, China.
Lu ZhangScience and Experiment Research Center, Shenyang Medical College, Shenyang, China.
Ming-Sheng ZhouSchool of Basic Medicine, Shenyang Medical College, Shenyang, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: This study investigated the role of Mzb1 in puerarin protection against heart injury and dysfunction in acute myocardial infarction (AMI) mice. Methods: C57BL/6 mice were pretreated with and without puerarin at doses of 50 mg/kg and 100 mg/kg for 14 days before establishing the AMI model. An AMI model was induced by ligating the left descending anterior coronary artery, and AC16 cardiomyocytes were treated with H Results: Puerarin dose-dependently reduced myocardial infarction area and injury, accompanied by the improvement of cardiac function in AMI mice. AMI mice manifested an increase in myocardial oxidative stress, endoplasmic reticulum (ER) stress, apoptosis, and mitochondrial biogenesis dysfunction, which were inhibited by pretreatment with puerarin. Puerarin also prevented Mzb1 downregulation in the hearts of AMI mice or H Conclusion: These results suggest that puerarin can protect against cardiac injury by attenuating oxidative stress and endoplasmic reticulum stress through upregulating the KLF4/Mzb1 pathway and that puerarin may expand our armamentarium for the prevention and treatment of ischemic heart diseases.

Indexed as

acute myocardial infarctionendoplasmic reticulummitochondria functionMzb1puerarin

Identifiers

PMID39206261
PMCPMC11350615

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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.