Evidence map›Paper›PMID 34591118›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2021

NORAD lentivirus shRNA mitigates fibrosis and inflammatory responses in diabetic cardiomyopathy via the ceRNA network of NORAD/miR-125a-3p/Fyn.

Ye Liu, Yikun Zhu, Sujun Liu, Jiong Liu, Xing Li

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In one paragraph

Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
–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

15 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Review
  4. Heart failure with preserved ejection fraction in pigs causes shifts in posttranscriptional checkpoints.American journal of physiology. Heart and circulatory physiology · 2024
    Article
  5. Article
  6. Roles of non-coding RNA in diabetic cardiomyopathy.Cardiovascular diabetology · 2024
    Review
  7. Epigenetics in diabetic cardiomyopathy.Clinical epigenetics · 2024
    Review
  8. Article
  9. Construction of a potentially functional long noncoding RNA-microRNA-mRNA network in diabetic cardiomyopathy.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2024
    Article
  10. Article
  11. Article
  12. Article
  13. Review
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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

5 authors.

Ye LiuDepartment of Endocrinology, The Second Hospital of ShanXi Medical University, 382 Wuyi Road, Taiyuan, 030001, Shanxi, China.
Yikun ZhuDepartment of Endocrinology, The Second Hospital of ShanXi Medical University, 382 Wuyi Road, Taiyuan, 030001, Shanxi, China.
Sujun LiuDepartment of Endocrinology, The Second Hospital of ShanXi Medical University, 382 Wuyi Road, Taiyuan, 030001, Shanxi, China.
Jiong LiuDepartment of Nuclear Medicine, The Second Hospital of ShanXi Medical University, 382 Wuyi Road, Taiyuan, 030001, Shanxi, China.
Xing LiDepartment of Endocrinology, The Second Hospital of ShanXi Medical University, 382 Wuyi Road, Taiyuan, 030001, Shanxi, China. xingl0220@163.com.ORCID http://orcid.org/0000-0002-1764-2988

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveDiabetic cardiomyopathy (DCM) is a serious complication of diabetes, but its pathogenesis is still unclear. This study investigated the mechanism of long noncoding RNA (lncRNA) NORAD in DCM.

methodsMale leptin receptor-deficient (db/db) mice and leptin control mice (db/ +) were procured. DCM model was established by subcutaneous injection of angiotensin II (ATII) in db/db mice. NORAD lentivirus shRNA or Adv-miR-125a-3p was administered to analyze cardiac function, fibrosis, serum biochemical indexes, inflammation and fibrosis. Primary cardiomyocytes were extracted and transfected with miR-125a-3p mimic. The competing endogenous RNA (ceRNA) network of NORAD/miR-125a-3p/Fyn was verified. The levels of fibrosis- and inflammation-related factors were measured.

resultsIn db/db mice treated with ATII, the body weight and serum biochemical indexes were increased, while the cardiac function was decreased, and inflammatory cell infiltration and fibrosis were induced. NORAD was upregulated in diabetic and DCM mice. The 4-week intravenous injection of NORAD lentivirus shRNA reduced body weight and serum biochemical indexes, improved cardiac function, and attenuated inflammation and fibrosis in DCM mice. NORAD acted as a sponge to adsorb miR-125a-3p, and miR-125a-3p targeted Fyn. Intravenous injection of miR-125a-3p adenovirus improved cardiac function and fibrosis and reduced inflammatory responses in DCM mice. Co-overexpression of miR-125-3p and Fyn partly reversed the improving effect of miR-125-3p overexpression on cardiac fibrosis in DCM mice.

conclusionNORAD lentivirus shRNA improved cardiac function and fibrosis and reduced inflammatory responses in DCM mice via the ceRNA network of NORAD/miR-125a-3p/Fyn. These findings provide a valuable and promising therapeutic target for the treatment of DCM.

Indexed as

MicroRNAsRNA, Long NoncodingAnimalsCytokinesDiabetic CardiomyopathiesFibrosisInflammationLentivirusMaleMiceMice, KnockoutMyocardiumProto-Oncogene Proteins c-fynReceptors, LeptinRNA, Small InterferingVentricular Function, LeftCytokinesFyn protein, mouseleptin receptor, mouseMicroRNAsMirn125 microRNA, mouseProto-Oncogene Proteins c-fynReceptors, LeptinRNA, Long NoncodingRNA, Small InterferingDiabetic cardiomyopathyFibrosisFynInflammationLncRNA NORADmiR-125a-3p

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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.