Evidence map›Paper›PMID 32212062›Full record

ArticleCardiovascular drugs and therapy2020

Dihydromyricetin Prevents Diabetic Cardiomyopathy via miR-34a Suppression by Activating Autophagy.

Tingjuan Ni, Na Lin, Wenqiang Lu, Zhenzhu Sun, Hui Lin, Jufang Chi, Hangyuan Guo

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Article in Cardiovascular drugs and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 2 pooled it
10.9field-weighted citation impact, top 1% 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

42 citing papers in PubMed, 2 syntheses or guidelines pooled it, 68 citations in OpenAlex.

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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.

Tingjuan NiZhejiang University, Hangzhou, Zhejiang, China.
Na LinZhejiang University, Hangzhou, Zhejiang, China.
Wenqiang LuZhejiang University, Hangzhou, Zhejiang, China.
Zhenzhu SunZhejiang University, Hangzhou, Zhejiang, China.
Hui LinZhejiang University, Hangzhou, Zhejiang, China.
Jufang ChiMedical Research Center, Shaoxing People's Hospital Shaoxing Hospital, Zhejiang University School of Medicine, No. 568 Zhongxing North Road, Shaoxing, Zhejiang, China. jufangc@163.com.ORCID https://orcid.org/0000-0002-3489-6023
Hangyuan GuoMedical Research Center, Shaoxing People's Hospital Shaoxing Hospital, Zhejiang University School of Medicine, No. 568 Zhongxing North Road, Shaoxing, Zhejiang, China. ghangyuan@hotmail.com.ORCID https://orcid.org/0000-0001-6980-1736
Zhejiang University · CNShaoxing People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeThe pro-aging miRNA, miR-34a, is hyperactivated in the cardiac myocardial tissues of patients and mice with diabetes, leading to diabetic cardiomyopathy (DCM). Increasing evidence suggests that dihydromyricetin (DHM) can be used to effectively treat cardiomyopathy. In this study, we investigated whether DHM affects the expression of miR-34a in DCM.

methodsThe expression of miR-34a in high-glucose-induced cardiomyocytes and in the heart tissue of diabetic mice was determined by microRNA isolation and quantitative reverse transcription-polymerase chain reaction. Lipofectamine 3000 was used to transfect cardiomyocytes with miR-34a inhibitor, miR-34a mimics, and miR-control. These agents were intravenously injected into the tail vein of streptozotocin-induced diabetic mice. Autophagy and apoptosis were assessed in high-glucose-induced cardiomyocytes and cardiac tissue in diabetic mice by western blotting, immunofluorescence, Masson staining, hematoxylin and eosin staining (H&E), and electron microscopy.

resultsDHM clearly ameliorated the cardiac dysfunction in the diabetic mice. The expression of miR-34a was up-regulated in high-glucose-induced cardiomyocytes and in the hearts of diabetic mice, thus impairing autophagy. Treatment with DHM decreased the expression of miR-34a and rescued the impairment of autophagy in high-glucose-induced cardiomyocytes and in the heart tissue of diabetic mice, while the miR-34a mimic offset the effect of DHM with respect to the development of DCM by inhibiting autophagy.

conclusionsBy decreasing the expression of miR-34a, DHM restores impaired autophagy, and thus ameliorates DCM. Therefore, DHM may potentially be used in the treatment of DCM.

Indexed as

AnimalsApoptosisAutophagyAutophagy-Related ProteinsCells, CulturedDiabetes Mellitus, ExperimentalDiabetic CardiomyopathiesDown-RegulationFlavonolsMaleMiceMicroRNAsMyocytes, CardiacRats, WistarSignal TransductionVentricular Function, LeftAutophagy-Related ProteinsdihydromyricetinFlavonolsMicroRNAsMIRN34a microRNA, mouseMIRN34 microRNA, ratAutophagyDiabetesDiabetic cardiomyopathyDihydromyricetinmiR-34a

Identifiers

PMID32212062
OpenAlexW3013783765

What OpenQuestion holds

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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.