Evidence map›Paper›PMID 31497222›Full record

ArticleAmerican journal of translational research2019

Endophilin A2 attenuates cardiac hypertrophy induced by isoproterenol through the activation of autophagy.

Xin-Qiu-Yue Wang, Zong-Tang Xu, Gui-Ping Zhang, Ning Hou, Qin-Xing Mo, Jie Wei, Xin Jiang, Yun Liu, Jian-Dong Luo

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

Article in American journal of translational research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.3field-weighted citation impact, top 40% 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

6 citing papers in PubMed, 7 citations in OpenAlex.

  1. 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 2 institutions in 1 country.

Xin-Qiu-Yue WangKey Laboratory of Molecular Target and Clinical Pharmacology and The State Key Laboratory of Respiratory Disease, School of Pharmaceutical Sciences and The Fifth Affiliated Hospital, Guangzhou Medical University Guangzhou 511436, Guangdong, P. R. China.
Zong-Tang XuKey Laboratory of Molecular Target and Clinical Pharmacology and The State Key Laboratory of Respiratory Disease, School of Pharmaceutical Sciences and The Fifth Affiliated Hospital, Guangzhou Medical University Guangzhou 511436, Guangdong, P. R. China.
Gui-Ping ZhangKey Laboratory of Molecular Target and Clinical Pharmacology and The State Key Laboratory of Respiratory Disease, School of Pharmaceutical Sciences and The Fifth Affiliated Hospital, Guangzhou Medical University Guangzhou 511436, Guangdong, P. R. China.
Ning HouKey Laboratory of Molecular Target and Clinical Pharmacology and The State Key Laboratory of Respiratory Disease, School of Pharmaceutical Sciences and The Fifth Affiliated Hospital, Guangzhou Medical University Guangzhou 511436, Guangdong, P. R. China.
Qin-Xing MoKey Laboratory of Molecular Target and Clinical Pharmacology and The State Key Laboratory of Respiratory Disease, School of Pharmaceutical Sciences and The Fifth Affiliated Hospital, Guangzhou Medical University Guangzhou 511436, Guangdong, P. R. China.
Jie WeiKey Laboratory of Molecular Target and Clinical Pharmacology and The State Key Laboratory of Respiratory Disease, School of Pharmaceutical Sciences and The Fifth Affiliated Hospital, Guangzhou Medical University Guangzhou 511436, Guangdong, P. R. China.
Xin JiangKey Laboratory of Molecular Target and Clinical Pharmacology and The State Key Laboratory of Respiratory Disease, School of Pharmaceutical Sciences and The Fifth Affiliated Hospital, Guangzhou Medical University Guangzhou 511436, Guangdong, P. R. China.
Yun LiuKey Laboratory of Molecular Target and Clinical Pharmacology and The State Key Laboratory of Respiratory Disease, School of Pharmaceutical Sciences and The Fifth Affiliated Hospital, Guangzhou Medical University Guangzhou 511436, Guangdong, P. R. China.
Jian-Dong LuoDepartment of Pharmacology, Guangzhou Institute of Cardiovascular Disease, Guangzhou Key Laboratory of Cardiovascular Disease, and The Second Affiliated Hospital, Guangzhou Medical University Guangzhou 510260, Guangdong, P. R. China.
State Key Laboratory of Respiratory Disease · CNSecond Affiliated Hospital of Guangzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Decreased autophagy has been reported to contribute to the progression of cardiac hypertrophy. Our previous research has demonstrated that endophilin A2 (EndoA2) attenuates H

Indexed as

autophagycardiac hypertrophyEndophilin A2isoproterenol

Identifiers

PMID31497222
PMCPMC6731414
OpenAlexW2987445678

What OpenQuestion holds

Textmetadata
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.