Evidence map›Paper›PMID 30748104›Full record

ArticleThe FEBS journal2019

Long noncoding RNA Crnde attenuates cardiac fibrosis via Smad3-Crnde negative feedback in diabetic cardiomyopathy.

Dezhi Zheng, Yong Zhang, Yonghe Hu, Jing Guan, Lianbin Xu, Wenjing Xiao, Qinyue Zhong, Chao Ren, Jinfeng Lu, Jiali Liang and 1 more

Open access · hybridAbstract readEditorial
In one paragraph

Article in The FEBS journal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
4.4field-weighted citation impact, top 4% 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

50 citing papers in PubMed, 84 citations in OpenAlex.

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  12. Epigenetics in diabetic cardiomyopathy.Clinical epigenetics · 2024
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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

11 authors at 2 institutions in 1 country.

Dezhi ZhengDepartment of Cardiovascular Surgery, The 960th Hospital of the PLA Joint Logistic Support Force, Jinan, China.
Yong ZhangDepartment of Cardiovascular Surgery, The 960th Hospital of the PLA Joint Logistic Support Force, Jinan, China.
Yonghe HuDepartment of Pharmacy, The General Hospital of Western Theater Command, Chengdu, China.
Jing GuanDepartment of Radiology, The General Hospital of Western Theater Command, Chengdu, China.
Lianbin XuDepartment of Cardiovascular Surgery, The 960th Hospital of the PLA Joint Logistic Support Force, Jinan, China.
Wenjing XiaoDepartment of Pharmacy, The General Hospital of Western Theater Command, Chengdu, China.
Qinyue ZhongDepartment of Pharmacy, The General Hospital of Western Theater Command, Chengdu, China.
Chao RenDepartment of Cardiovascular Surgery, The 960th Hospital of the PLA Joint Logistic Support Force, Jinan, China.
Jinfeng LuDepartment of Cardiovascular Surgery, The 960th Hospital of the PLA Joint Logistic Support Force, Jinan, China.
Jiali LiangDepartment of Cardiovascular Surgery, The 960th Hospital of the PLA Joint Logistic Support Force, Jinan, China.
Jun HouDepartment of Pharmacy, The General Hospital of Western Theater Command, Chengdu, China.
People's Liberation Army 401 Hospital · CNChengdu Military General Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic cardiomyopathy (DCM)-ventricular dysfunction in the absence of underlying heart disease-is a common complication of diabetes and a leading cause of mortality associated with the disease. In DCM, cardiac fibrosis is the main cause of heart failure. Although it is well-established that the transforming growth factor-beta signaling pathway plays a part in inducing cardiac fibrosis in DCM, details of the molecular mechanism involved remain elusive. Therefore, it is crucial to study the gene reg;ulation of key signaling effectors in DCM-associated cardiac fibrosis. A recently emerged hotspot in the field of gene regulation is the role of long noncoding RNAs (lncRNAs). Recent evidence indicates that lncRNAs play a critical role in cardiac fibrosis; however, in DCM, the function of these regulatory RNAs have not been studied in depth. In this study, we identified a conserved cardiac-specific lncRNA named colorectal neoplasia differentially expressed (Crnde). By analyzing 376 human heart tissues, it was found that Crnde expression is negatively correlated with that of cardiac fibrosis marker genes. Moreover, Crnde expression was shown to be enriched in cardiac fibroblasts (CFs). Overexpression of Crnde attenuated cardiac fibrosis and enhanced cardiac function in mice with DCM. Further, in vitro experiments showed that Crnde negatively regulates the myofibroblast differentiation of CFs. The expression of Crnde was activated by SMAD family member 3 (Smad3), shedding light on the underlying molecular mechanism. Interestingly, Crnde also inhibited the transcriptional activation of Smad3 on target genes, thereby inhibiting the expression of myofibroblastic marker genes in CFs. Overall, our data provide valuable insights into the development of potential anti-cardiac fibrosis strategies centered on lncRNAs, for the treatment of DCM.

Indexed as

AnimalsDependovirusDiabetes Mellitus, ExperimentalDiabetic CardiomyopathiesFeedback, PhysiologicalFibroblastsFibrosisGene Expression RegulationGene Knockdown TechniquesHumansMaleMiceMice, Inbred C57BLMyocardiumOrgan SpecificityRNA, AntisenseCRNDE RNA, humanRNA, AntisenseRNA, Long NoncodingSmad3 ProteinSmad3 protein, mousecardiac fibrosisCrndediabetic cardiomyopathylong noncoding RNA

Identifiers

PMID30748104
PMCPMC6849551
OpenAlexW2914903642

What OpenQuestion holds

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LicenceCC BY
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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.