Evidence map›Paper›PMID 28744126›Full record

ArticleInternational journal of nanomedicine2017

Gold nanoparticle-based miR155 antagonist macrophage delivery restores the cardiac function in ovariectomized diabetic mouse model.

Chengming Jia, Hui Chen, Mengying Wei, Xiangjie Chen, Yajun Zhang, Liang Cao, Ping Yuan, Fangyuan Wang, Guodong Yang, Jing Ma

Open access · goldAbstract read
In one paragraph

Article in International journal of nanomedicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 2 pooled it
3.9field-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

53 citing papers in PubMed, 2 syntheses or guidelines pooled it, 101 citations in OpenAlex.

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  4. Role of miR-155 and miR-103 in Oxidative Stress in Cardiovascular Disease: A Narrative Review.Pathophysiology : the official journal of the International Society for Pathophysiology · 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

10 authors at 2 institutions in 1 country.

Chengming JiaDepartment of Chinese Medicine, Xijing Hospital, The Fourth Military Medical University, Xi'an, China.
Hui ChenDepartment of Plastic Surgery, Tangdu Hospital, The Fourth Military Medical University, Xi'an, China.
Mengying WeiDepartment of Biochemistry and Molecular Biology, The Fourth Military Medical University, Xi'an, China.
Xiangjie ChenDepartment of Mathematics, Southeast University, Nanjing, China.
Yajun ZhangDepartment of Ultrasound Diagnosis, Tangdu Hospital, The Fourth Military Medical University, Xi'an, China.
Liang CaoDepartment of Chinese Medicine, Xijing Hospital, The Fourth Military Medical University, Xi'an, China.
Ping YuanDepartment of Chinese Medicine, Xijing Hospital, The Fourth Military Medical University, Xi'an, China.
Fangyuan WangDepartment of Chinese Medicine, Xijing Hospital, The Fourth Military Medical University, Xi'an, China.
Guodong YangDepartment of Biochemistry and Molecular Biology, The Fourth Military Medical University, Xi'an, China.
Jing MaDepartment of Chinese Medicine, Xijing Hospital, The Fourth Military Medical University, Xi'an, China.
Air Force Medical University · CNSoutheast University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic cardiomyopathy is a common disease in postmenopausal women, in whom the estrogen deficiency aggravates the pathology. In this study, we have found that estrogen deficiency due to ovariectomy aggravates the inflammation in the hearts of diabetic mice, as depicted by excessive proinflammatory type 1 macrophages (M1) over anti-inflammatory type 2 macrophages (M2). Accordingly, an additional increase of reactive oxygen species, cell apoptosis, cardiac hypertrophy, and fibrosis was observed in the hearts of ovariectomized diabetic mice, in comparison with the diabetes-only group. Significantly, miR155, a potent promoter of M1 polarization, was found to be additionally enhanced in the macrophages and hearts by ovariectomy. Tail vein injection of miR155-AuNP, in which thiol-modified antago-miR155 was covalently conjugated with gold nanoparticle (AuNP), preferentially delivered the nucleic acids into the macrophages via phagocytosis. Together with the increased M2 ratio and reduced inflammation, in vivo delivery of antago-miR155 reduced cell apoptosis and restored the cardiac function. The restoration efficacy of miR155-AuNP was much better than general macrophage depletion by clodrosome. In summary, we revealed that M1/M2 imbalance contributes to the aggravated cardiomyopathy in ovariectomized diabetic mice, and therapeutically reducing miR155 in macrophages by AuNP serves as a promising strategy in improving cardiac function.

Indexed as

AnimalsApoptosisDiabetes Mellitus, ExperimentalDiabetic CardiomyopathiesDrug Delivery SystemsFemaleFibrosisGoldMacrophagesMice, Inbred C57BLMicroRNAsMyocarditisMyocardiumNanoparticlesOvariectomyGoldMicroRNAsMirn155 microRNA, mousecardiac functiongold nanoparticlemacrophagemiR155ovariectomized diabetic mouse modeltargeted delivery

Identifiers

PMID28744126
PMCPMC5513843
OpenAlexW2735256643

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.