Evidence map›Paper›PMID 32061268›Full record

ArticleMolecular therapy : the journal of the American Society of Gene Therapy2020

The 3' Untranslated Region Protects the Heart from Angiotensin II-Induced Cardiac Dysfunction via AGGF1 Expression.

Lexi Ding, Shan Lu, Yu Zhou, Dayin Lyu, Changhan Ouyang, Zejun Ma, Qiulun Lu

Open access · greenAbstract read
In one paragraph

Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
0.6field-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

28 citing papers in PubMed, 24 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 5 institutions in 2 countries.

Lexi DingDepartment of Ophthalmology, Xiangya Hospital, Central South University, Changsha, China.
Shan LuDepartment of Pharmacology, University of California, Davis, Davis, CA, USA.
Yu ZhouKey Laboratory of Cardiovascular and Cerebrovascular Medicine, School of Pharmacy, Nanjing Medical University, Nanjing 211166, China.
Dayin LyuKey Laboratory of Cardiovascular and Cerebrovascular Medicine, School of Pharmacy, Nanjing Medical University, Nanjing 211166, China.
Changhan OuyangDepartment of Pharmacy, Hubei Key Laboratory of Diabetes and Angiopathy, Hubei University of Science and Technology, Xianning 437100, China.
Zejun MaNHC Key Laboratory of Hormones and Development (Tianjin Medical University), Tianjin Key Laboratory of Metabolic Diseases, Tianjin Medical University Chu Hsien-I Memorial Hospital and Tianjin Institute of Endocrinology, Tianjin 300134, China.
Qiulun LuKey Laboratory of Cardiovascular and Cerebrovascular Medicine, School of Pharmacy, Nanjing Medical University, Nanjing 211166, China. Electronic address: qiulunlu@njmu.edu.cn.
Nanjing Medical University · CNCentral South University · CNHubei University of Science and Technology · CNTianjin Medical University · CNUniversity of California, Davis · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The messenger RNA (mRNA) 3' untranslated regions (3' UTRs), as cis-regulated elements bound by microRNAs (miRNAs), affect their gene translation. However, the role of the trans-regulation of 3' UTRs during heart dysfunction remains elusive. Compared with administration of angiogenic factor with G-patch and forkhead-associate domains 1 (Aggf1), ectopic expression of Aggf1 with its 3' UTR significantly suppressed cardiac dysfunction in angiotensin II-infused mice, with upregulated expression of both Aggf1 and myeloid cell leukemia 1 (Mcl1). Along their 3' UTRs, Mcl1 and Aggf1 mRNAs share binding sites for the same miRNAs, including miR-105, miR-101, and miR-93. We demonstrated that the protein-coding Mcl1 and Aggf1 mRNAs communicate and co-regulate each other's expression through competition for these three miRNAs that target both transcripts via their 3' UTRs. Our results indicate that Aggf1 3' UTR, as a trans-regulatory element, accelerates the cardioprotective role of Aggf1 in response to hypertensive conditions by elevating Mcl1 expression. Our work broadens the scope of gene therapy targets and provides a new insight into gene therapy strategies involving 3' UTRs.

Indexed as

3' Untranslated RegionsAngiogenic ProteinsAngiotensin IIAnimalsCells, CulturedDependovirusDisease Models, AnimalGenetic TherapyGenetic VectorsHeart DiseasesHeart Function TestsHEK293 CellsHumansMaleMiceMicroRNAs3' Untranslated RegionsAggf1 protein, mouseAngiogenic ProteinsAngiotensin IIMcl1 protein, mouseMicroRNAsMIRN101 microRNA, mouseMirn93 microRNA, mouseMyeloid Cell Leukemia Sequence 1 Protein3’UTRAGGF1cardiac dysfunctionMCL1

Identifiers

PMID32061268
PMCPMC7132794
OpenAlexW3005059497

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.