Evidence map›Paper›PMID 34607973›Full record

ArticleAging2021

Allicin protects against myocardial I/R by accelerating angiogenesis via the miR-19a-3p/PI3K/AKT axis.

Mengru Liu, Peng Yang, Dongliang Fu, Tong Gao, Xinyi Deng, Mingjing Shao, Jiangquan Liao, Hong Jiang, Xianlun Li

Open access · hybridAbstract read
In one paragraph

Article in Aging, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
5.5field-weighted citation impact, top 5% 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

23 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
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  7. mTOR Signaling in Macrophages: All Depends on the Context.International journal of molecular sciences · 2025
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  11. LINC01271 promotes fracture healing via regulating miR-19a-3p/PIK3CA axis.Journal of orthopaedic surgery and research · 2025
    Article
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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

9 authors at 3 institutions in 1 country.

Mengru LiuGraduate School of Peking Union Medical College, Beijing 100730, China.
Peng YangDepartment of Integrative Medicine Cardiology, China-Japan Friendship Hospital, Beijing 100029, China.
Dongliang FuDepartment of Integrative Medicine Cardiology, China-Japan Friendship Hospital, Beijing 100029, China.
Tong GaoGraduate School of Peking Union Medical College, Beijing 100730, China.
Xinyi DengDepartment of Integrative Medicine Cardiology, China-Japan Friendship Hospital, Beijing 100029, China.
Mingjing ShaoDepartment of Integrative Medicine Cardiology, China-Japan Friendship Hospital, Beijing 100029, China.
Jiangquan LiaoDepartment of Integrative Medicine Cardiology, China-Japan Friendship Hospital, Beijing 100029, China.
Hong JiangDepartment of Integrative Medicine Cardiology, China-Japan Friendship Hospital, Beijing 100029, China.
Xianlun LiGraduate School of Peking Union Medical College, Beijing 100730, China.
China-Japan Friendship Hospital · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNPeking Union Medical College Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesAllicin is an allyl 2-propenethiosulfinate or diallyl thiosulfinate acid with cardioprotective effects in myocardial ischemia/reperfusion (MI/R) injury. This study aims to examine the underlying mechanism by which Allicin protects against MI/R.

methodsC57BL6 mice were subjected to either sham or MI/R surgery, and mice in the Allicin group were injected with Allicin (5 mg/ml) before the induction of ischemia. The cardiac function and histopathology of experimental mice were evaluated by ultrasound quantification and Masson staining. We next measured the capillary angiogenesis of the peri-infarct area by Masson staining and immunohistochemical staining. The miRNA microarray was carried out to examine the expressed miRNAs in MI/R tissues and corresponding normal tissues. Real-time quantitative polymerase chain reaction (q-PCR) was performed to validate the selected miRNA-19α-3p gene expression. Besides, we evaluated the myocardial lactate dehydrogenase and COX-2 by immunofluorescence staining. The western blot analysis was used to evaluate the protein levels of p-AKT, p-PI3K, p-mTOR, COX-2, and VEGF protein in the Allicin and Model group.

resultsAllicin pretreatment significantly improved I/R-induced cardiac function damage. Furthermore, Allicin could repress cardiac fibrosis, as evidenced by reduced areas of cardiac fibrosis. Allicin's effect on the MI/R was associated with increased capillary angiogenesis. Microarray analysis exposed that miR-19a-3p down-regulated PIK3CA (PI3K) expression by directly targeting the PIK3CA gene. The regulation of the angiogenesis pathway and gene miRNA-19a-3p might affect the Allicin-induced MI/R protection. Immunofluorescence staining revealed that COX-2 and myocardial lactate dehydrogenase were significantly increased after Allicin treatment. Furthermore, western blot analysis demonstrated that p-AKT, p-PI3K, p-mTOR, COX-2, and VEGF protein levels were also increased in the Allicin group.

conclusionsAllicin pretreatment protects against myocardial I/R and activating the miR-19a-3p/PI3K/AKT pathway.

Indexed as

AnimalsCells, CulturedCyclooxygenase 2DisulfidesGene Expression RegulationL-Lactate DehydrogenaseMacrophagesMaleMiceMicroRNAsMyocardial IschemiaNeovascularization, PhysiologicPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReperfusion InjurySignal TransductionallicinCyclooxygenase 2DisulfidesL-Lactate DehydrogenaseMicroRNAsMIRN19A microRNA, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSulfinic AcidsVascular Endothelial Growth Factor Avascular endothelial growth factor A, mouseAllicinangiogenesismiR-19a-3pmyocardial I/RPI3K/AKT pathway

Identifiers

PMID34607973
PMCPMC8544308
OpenAlexW3202179639

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.