Evidence map›Paper›PMID 34146302›Full record

ArticleJournal of physiology and biochemistry2021

miR-124-3p targeted SIRT1 to regulate cell apoptosis, inflammatory response, and oxidative stress in acute myocardial infarction in rats via modulation of the FGF21/CREB/PGC1α pathway.

Yun-Jie Wei, Jun-Feng Wang, Fei Cheng, Hai-Jun Xu, Jia-Juan Chen, Jian Xiong, Jing Wang

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of physiology and biochemistry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

20 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
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  3. EV-Encapsulated Mitochondrial miRNAs: Enhancing Cardiomyocyte Bioenergetics.International journal of molecular sciences · 2026
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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

7 authors at 2 institutions in 1 country.

Yun-Jie WeiDepartment of Cardiology, Taihe Hospital, Hubei University of Medicine, Shiyan City, Hubei Province, China.
Jun-Feng WangDepartment of Cardiology, Taihe Hospital, Hubei University of Medicine, Shiyan City, Hubei Province, China.
Fei ChengDepartment of Cardiology, Taihe Hospital, Hubei University of Medicine, Shiyan City, Hubei Province, China.
Hai-Jun XuDepartment of Cardiology, Taihe Hospital, Hubei University of Medicine, Shiyan City, Hubei Province, China.
Jia-Juan ChenDepartment of Cardiology, Taihe Hospital, Hubei University of Medicine, Shiyan City, Hubei Province, China.
Jian XiongDepartment of Cardiology, Taihe Hospital, Hubei University of Medicine, Shiyan City, Hubei Province, China.
Jing WangDepartment of Neurology, Taihe Hospital, Hubei University of Medicine, No. 32, South Renmin Road, Shiyan City, 442000, Hubei Province, China. eleven190708@sina.com.
Hubei University of Medicine · CNTaihe Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To investigate whether miR-124-3p influences cell apoptosis, inflammatory response, and oxidative stress in rats with acute myocardial infarction (AMI) by mediating the SIRT1/FGF21/CREB/PGC1α pathway. A dual-luciferase reporter gene assay was performed to verify the relationship between miR-124-3p and SIRT1. AMI rats were established via coronary artery ligation after injection with agomiR-124-3p, antagomiR-124-3p, and/or SIRT1 siRNA, and triphenyltetrazolium chloride (TTC), HE, and TUNEL stainings were performed. Bio-Plex rat cytokine assays were performed to determine proinflammatory factor levels. qRT-PCR and Western blotting were used to examine the mRNA and protein expression, respectively. The activity levels of antioxidant enzymes in myocardial tissues were also measured. miR-124-3p was confirmed to target SIRT1 in the H9C2 cells. AMI rats exhibited increased miR-124-3p expression and decreased SIRT1 expression in myocardial tissues. HE staining showed a disorganized cell arrangement and inflammatory cell infiltration in the myocardial tissues of the AMI rats, which was more severe in the rats injected with SIRT1 and agomiR-124-3p but was ameliorated in those treated with antagomiR-124-3p. Moreover, the AMI rats in the antagomiR-124-3p group presented with a reduction in infarct area with an increase in antioxidant enzyme activity, Bcl-2 expression, and activation of the FGF21/CREB/PGC1α pathway, as well as a decrease in cell apoptosis rate, Bax and Caspase-3 expression, and levels of proinflammatory factors, effects that were reversed by si-SIRT1. Inhibiting miR-124-3p expression may activate the FGF21/CREB/PGC1α pathway to reduce cell apoptosis, alleviate the inflammatory response, and attenuate oxidative stress in AMI rats by targeting SIRT1. Graphical abstract.

Indexed as

MicroRNAsMyocardial InfarctionAnimalsApoptosisFibroblast Growth FactorsOxidative StressPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPyroptosisRatsRats, Sprague-DawleySirtuin 1fibroblast growth factor 21Fibroblast Growth FactorsMicroRNAsMIRN124 microRNA, ratPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaSirt1 protein, ratSirtuin 1AMIFGF21/CREB/PGC1αmiR-124-3pSIRT1

Identifiers

PMID34146302
OpenAlexW3168360017

What OpenQuestion holds

Textmetadata
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.