Evidence map›Paper›PMID 28811357›Full record

ArticleBioscience reports2017

Autophagy attenuates endothelial-to-mesenchymal transition by promoting Snail degradation in human cardiac microvascular endothelial cells.

Jin Zou, Yanhua Liu, Bingong Li, Zeqi Zheng, Xuan Ke, Yanqin Hao, Xuelian Li, Xingxing Li, Fuyou Liu, Zhiyong Zhang

Abstract read
In one paragraph

Article in Bioscience reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
–field-weighted citation impact
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

31 citing papers in PubMed.

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  19. Autophagy attenuates renal fibrosis in obstructive nephropathy through inhibiting epithelialZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2021
    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

10 authors.

Jin ZouDepartment of Cardiology, First Affiliated Hospital, Nanchang University, Nanchang 330006, Jiangxi Province, China.
Yanhua LiuDepartment of Cardiology, Loudi Central Hospital, Loudi 417000, Hunan Province, China.
Bingong LiDepartment of Cardiology, First Affiliated Hospital, Nanchang University, Nanchang 330006, Jiangxi Province, China libingong08@163.com.
Zeqi ZhengDepartment of Cardiology, First Affiliated Hospital, Nanchang University, Nanchang 330006, Jiangxi Province, China.
Xuan KeDepartment of Cardiology, First Affiliated Hospital, Nanchang University, Nanchang 330006, Jiangxi Province, China.
Yanqin HaoDepartment of Cardiology, First Affiliated Hospital, Nanchang University, Nanchang 330006, Jiangxi Province, China.
Xuelian LiDepartment of Cardiology, First Affiliated Hospital, Nanchang University, Nanchang 330006, Jiangxi Province, China.
Xingxing LiDepartment of Cardiology, First Affiliated Hospital, Nanchang University, Nanchang 330006, Jiangxi Province, China.
Fuyou LiuDepartment of Cardiology, First Affiliated Hospital, Nanchang University, Nanchang 330006, Jiangxi Province, China.
Zhiyong ZhangDepartment of Cardiology, First Affiliated Hospital, Nanchang University, Nanchang 330006, Jiangxi Province, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endothelial-to-mesenchymal transition (EndMT) mainly exists in cardiovascular development and disease progression, and is well known to contribute to cardiac fibrosis. Recent studies indicated that autophagy also participates in the regulation of cardiac fibrosis. However, the precise role of autophagy in cardiac fibrosis and the underlying molecular mechanism remain unclear. The present study aimed to explore the role of autophagy in EndMT, reveal the underlying molecular mechanism, and seek new therapy for cardiac fibrosis. In the present study, we found that EndMT and autophagy were induced simultaneously by hypoxia in human cardiac microvascular endothelial cells (HCMECs). Rapamycin, an autophagy enhancer, attenuated EndMT with promoting angiogenesis, while 3-methyladenine (3-MA) and chloroquine (CQ), agents that inhibit autophagy, accelerated the progression accompanied by the decrease in counts of tube formation under hypoxia conditions. Interestingly, intervening autophagy by rapamycin, 3-MA, or CQ did not affect hypoxia-induced autocrine TGFβ signaling, but changed the expression of Snail protein without alterations in the expression of

Indexed as

AutophagyEpithelial-Mesenchymal TransitionCell HypoxiaCell LineCoronary VesselsEndothelial CellsHumansMicrovesselsProteolysisSnail Family Transcription FactorsSnail Family Transcription Factorsautophagyhypoxiandothelial-to-mensenchymal transitionSnailTGFβ2

Identifiers

PMID28811357
PMCPMC5587916

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.