Evidence map›Paper›PMID 35703318›Full record

ArticleBioengineered2022

lncRNA NBR2 attenuates angiotensin II-induced myocardial hypertrophy through repressing ER stress via activating LKB1/AMPK/Sirt1 pathway.

Cansheng Zhu, Min Wang, Xianguan Yu, Xing Shui, Leile Tang, Zefeng Chen, Zhaojun Xiong

Open access · goldAbstract read
In one paragraph

Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

14 citing papers in PubMed, 18 citations in OpenAlex.

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  13. Noncoding RNAs as Key Regulators for Cardiac Development and Cardiovascular Diseases.Journal of cardiovascular development and disease · 2023
    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

7 authors at 2 institutions in 1 country.

Cansheng ZhuDepartment of Neurology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China.
Min WangDepartment of Cardiovascular Internal Medicine, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China.
Xianguan YuDepartment of Cardiovascular Internal Medicine, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China.
Xing ShuiDepartment of Cardiovascular Internal Medicine, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China.
Leile TangDepartment of Cardiovascular Internal Medicine, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China.
Zefeng ChenDepartment of Cardiovascular Internal Medicine, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China.
Zhaojun XiongDepartment of Cardiovascular Internal Medicine, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China.
Third Affiliated Hospital of Sun Yat-sen University · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myocardial hypertrophy leads to heart failure (HF), and emerging researchers have illustrated that long noncoding RNAs (lncRNAs) modulate myocardial hypertrophy. Here, we explored the role and mechanism of a novel lncRNA, NBR2, in modulating angiotensin II (Ang II)-induced myocardial hypertrophy. First, we examined plasma NBR2 levels in 25 patients with HF and myocardial hypertrophy and ten healthy donors and analyzed the correlation between NBR2 profiles and patients' clinical indicators. In addition, the overexpression experiment of NBR2 was carried out to probe the influence of NBR2 on myocardial hypertrophy. lncRNA NBR2 was down-regulated in plasma of patients with HF and myocardial hypertrophy (vs. healthy controls), and its level was negatively correlated with cardiac function (represented by left ventricular end-diastolic diameter and left ventricular ejection fraction) and degree of myocardial hypertrophy. Besides, Ang II treatment intensified the hypertrophy of human myocardial cell lines (HCM and AC16) and curbed the NBR2 expression. Overexpressing lncRNA NBR2 alleviated Angiotension II-induced myocardial hypertrophy and declined the profiles of hypertrophic markers. Moreover, up-regulating lncRNA NBR2 weakened Ang II-mediated endoplasmic reticulum (ER) stress and activated the LKB1/AMPK/Sirt1 pathway. Interfering with the LKB1/AMPK/Sirt1 axis abated the lncRNA NBR2-mediated inhibitory effect on myocardial hypertrophy and ER stress. This study confirmed that lncRNA NBR2 dampened myocardial hypertrophy and ER stress by modulating the LKB1/AMPK/Sirt1 pathway. Our study provides the first evidence that lncRNA NBR2 is positively associated with myocardial hypertrophy.

Indexed as

RNA, Long NoncodingAMP-Activated Protein KinasesAngiotensin IIHumansHypertrophyMyocytes, CardiacSignal TransductionSirtuin 1Stroke VolumeVentricular Function, LeftAMP-Activated Protein KinasesAngiotensin IIRNA, Long NoncodingSIRT1 protein, humanSirtuin 1angiotensin IIEndoplasmic reticulum stresslncRNA NBR2myocardial hypertrophy

Identifiers

PMID35703318
PMCPMC9275985
OpenAlexW4282918341

What OpenQuestion holds

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LicenceCC BY
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.