Evidence map›Paper›PMID 36384975›Full record

ArticleBiology direct2022

LncRNA Airn alleviates diabetic cardiac fibrosis by inhibiting activation of cardiac fibroblasts via a m6A-IMP2-p53 axis.

Tingwei Peng, Mingchuan Liu, Lang Hu, Dong Guo, Di Wang, Bingchao Qi, Gaotong Ren, Chenchen Hu, Feng Zhang, Hyung J Chun and 3 more

Open access · goldAbstract read
In one paragraph

Article in Biology direct, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
4.6field-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

41 citing papers in PubMed, 53 citations in OpenAlex.

  1. Article
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  8. Advances in RNA modification in myocardial fibrosis (Review).International journal of molecular medicine · 2025
    Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. IMPlications of IMP2 in RNA Biology and Disease.International journal of molecular sciences · 2025
    Review
  16. Review
  17. Review
  18. 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

13 authors at 3 institutions in 2 countries.

Tingwei Peng *Department of Cardiology, Tangdu Hospital, The Fourth Military Medical University, Xi'an, 710038, People's Republic of China.
Mingchuan Liu *Department of Cardiology, Tangdu Hospital, The Fourth Military Medical University, Xi'an, 710038, People's Republic of China.
Lang Hu *Department of Cardiology, Tangdu Hospital, The Fourth Military Medical University, Xi'an, 710038, People's Republic of China.
Dong GuoDepartment of Cardiology, Tangdu Hospital, The Fourth Military Medical University, Xi'an, 710038, People's Republic of China.
Di WangDepartment of Cardiology, Tangdu Hospital, The Fourth Military Medical University, Xi'an, 710038, People's Republic of China.
Bingchao QiDepartment of Cardiology, Tangdu Hospital, The Fourth Military Medical University, Xi'an, 710038, People's Republic of China.
Gaotong RenDepartment of Cardiology, Tangdu Hospital, The Fourth Military Medical University, Xi'an, 710038, People's Republic of China.
Chenchen HuDepartment of Immunology, The Fourth Military Medical University, Xi'an, 710032, Shaanxi, People's Republic of China.
Feng ZhangState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-Sen University, Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science, Guangzhou, 510060, People's Republic of China.
Hyung J ChunYale Cardiovascular Research Center, Section of Cardiovascular Medicine, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, 06511, USA.
Liqiang SongDepartment of Pulmonary and Critical Care Medicine, Xijing Hospital, The Fourth Military Medical University, Xi'an, 710038, People's Republic of China.
Jianqiang HuDepartment of Cardiology, Tangdu Hospital, The Fourth Military Medical University, Xi'an, 710038, People's Republic of China. hujq0108@163.com.
Yan LiDepartment of Cardiology, Tangdu Hospital, The Fourth Military Medical University, Xi'an, 710038, People's Republic of China. profleeyan@163.com.
Air Force Medical University · CNSun Yat-sen University · CNYale University · US

Funding

Yale Clinical and Translational Science Award (U Component)UL1TR001863 · NCATS · YALE UNIVERSITY · PI John H. Krystal, LUCILA OHNO-MACHADO · 2016 to 2026
$102.9M
NCATS NIH HHS UL1 TR001863
6 · The paper itself

Abstract

backgroundCardiac fibrosis is a leading cause of cardiac dysfunction in patients with diabetes. However, the underlying mechanisms of cardiac fibrosis remain unclear. This study aimed to investigate the role of the long non-coding RNA (LncRNA) Airn in the pathogenesis of cardiac fibrosis in diabetic cardiomyopathy (DCM) and its underlying mechanism.

methodsDiabetes mellitus (DM) was induced in mice by streptozotocin injection. An intramyocardial adeno-associated virus (AAV) was used to manipulate Airn expression. The functional significance and underlying mechanisms in DCM fibrosis were investigated both in vitro and in vivo.

resultsDiabetic hearts showed a significant impairment in cardiac function, accompanied by obviously increased cardiac fibrosis. Interestingly, lncRNA Airn expression was significantly decreased in both diabetic hearts and high glucose (HG)-treated cardiac fibroblasts (CFs). AAV-mediated Airn reconstitution prevented cardiac fibrosis and the development of DCM, while Airn knockdown induced cardiac fibrosis phenotyping DCM. As in vitro, Airn reversed HG-induced fibroblast-myofibroblast transition, aberrant CFs proliferation and section of collagen I. In contrast, Airn knockdown mimicked a HG-induced CFs phenotype. Mechanistically, we identified that Airn exerts anti-fibrotic effects by directly binding to insulin-like growth factor 2 mRNA-binding protein 2 (IMP2) and further prevents its ubiquitination-dependent degradation. Moreover, we revealed that Airn/IMP2 protected p53 mRNA from degradation in m6A manner, leading to CF cell cycle arrest and reduced cardiac fibrosis. As a result, ablation of p53 blunted the inhibitory effects of Airn on fibroblast activation and cardiac fibrosis.

conclusionsOur study demonstrated for the first time that Airn prevented the development of cardiac fibrosis in diabetic heart via IMP2-p53 axis in an m6A dependent manner. LncRNA Airn could be a promising therapeutic target for cardiac fibrosis in DCM.

Indexed as

Diabetes MellitusDiabetic CardiomyopathiesRNA-Binding ProteinsRNA, Long NoncodingTumor Suppressor Protein p53AdenosineAnimalsFibroblastsFibrosisMiceRNA, MessengerAdenosineAir non-coding RNA, mouseIGF2BP2 protein, mouseN-methyladenosineRNA-Binding ProteinsRNA, Long NoncodingRNA, MessengerTumor Suppressor Protein p53Diabetic cardiomyopathyFibroblast proliferationFibrosisLncRNA-Airnm6A modificationP53

Identifiers

PMID36384975
PMCPMC9670606
OpenAlexW4309466102

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.