Evidence map›Paper›PMID 34518516›Full record

ArticleCell death & disease2021

Secretory products from epicardial adipose tissue induce adverse myocardial remodeling after myocardial infarction by promoting reactive oxygen species accumulation.

Shuang Hao, Xin Sui, Jing Wang, Jingchao Zhang, Yu Pei, Longhui Guo, Zhenxing Liang

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
5.5field-weighted citation impact, top 3% 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

29 citing papers in PubMed, 52 citations in OpenAlex.

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  4. The pathophysiological role of MiRNAs in heart failure.Frontiers in cardiovascular medicine · 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 1 institution in 1 country.

Shuang HaoDepartment of Cardiac Surgery, The First Affiliated Hospital of Zhengzhou University, 450000, Zhengzhou, China. haoshuang89@hotmail.com.ORCID 0000-0002-8638-2956
Xin SuiDepartment of Oncology, The First Affiliated Hospital of Zhengzhou University, 450000, Zhengzhou, China.
Jing WangDepartment of Cardiac Surgery, The First Affiliated Hospital of Zhengzhou University, 450000, Zhengzhou, China.
Jingchao ZhangDepartment of Cardiac Surgery, The First Affiliated Hospital of Zhengzhou University, 450000, Zhengzhou, China.
Yu PeiDepartment of Cardiac Surgery, The First Affiliated Hospital of Zhengzhou University, 450000, Zhengzhou, China.
Longhui GuoDepartment of Cardiac Surgery, The First Affiliated Hospital of Zhengzhou University, 450000, Zhengzhou, China.
Zhenxing LiangDepartment of Cardiac Surgery, The First Affiliated Hospital of Zhengzhou University, 450000, Zhengzhou, China.
First Affiliated Hospital of Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Adverse myocardial remodeling, manifesting pathologically as myocardial hypertrophy and fibrosis, often follows myocardial infarction (MI) and results in cardiac dysfunction. In this study, an obvious epicardial adipose tissue (EAT) was observed in the rat model of MI and the EAT weights were positively correlated with cardiomyocyte size and myocardial fibrosis areas in the MI 2- and 4-week groups. Then, rat cardiomyocyte cell line H9C2 and primary rat cardiac fibroblasts were cultured in conditioned media generated from EAT of rats in the MI 4-week group (EAT-CM). Functionally, EAT-CM enlarged the cell surface area of H9C2 cells and reinforced cardiac fibroblast activation into myofibroblasts by elevating intracellular reactive oxygen species (ROS) levels. Mechanistically, miR-134-5p was upregulated by EAT-CM in both H9C2 cells and primary rat cardiac fibroblasts. miR-134-5p knockdown promoted histone H3K14 acetylation of manganese superoxide dismutase and catalase by upregulating lysine acetyltransferase 7 expression, thereby decreasing ROS level. An in vivo study showed that miR-134-5p knockdown limited adverse myocardial remodeling in the rat model of MI, manifesting as alleviation of cardiomyocyte hypertrophy and fibrosis. In general, our study clarified a new pathological mechanism involving an EAT/miRNA axis that explains the adverse myocardial remodeling occurring after MI.

Indexed as

Ventricular RemodelingAdipose TissueAnimalsCardiomegalyCell LineDisease Models, AnimalFibroblastsFibrosisGene Expression ProfilingGene Expression RegulationHistone AcetyltransferasesMaleMicroRNAsMyocardial InfarctionMyocardiumMyocytes, CardiacHistone AcetyltransferasesKat7 protein, ratMicroRNAsMIRN134 microRNA, ratReactive Oxygen SpeciesSuperoxide Dismutase

Identifiers

PMID34518516
PMCPMC8438091
OpenAlexW3201530379

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.