Evidence map›Paper›PMID 34953026›Full record

ArticleJournal of cellular and molecular medicine2022

Thymoquinone ameliorates pressure overload-induced cardiac hypertrophy by activating the AMPK signalling pathway.

Heng Chen, Chengui Zhuo, Aohan Zu, Shuai Yuan, Han Zhang, Jianqiang Zhao, Liangrong Zheng

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

13 citing papers in PubMed, 20 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 3 institutions in 1 country.

Heng ChenDepartment of Cardiology and Atrial Fibrillation Center, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China.
Chengui ZhuoDepartment of Cardiology, Taizhou Central Hospital (Taizhou University Hospital), Taizhou, Zhejiang, China.
Aohan ZuDepartment of Cardiology and Atrial Fibrillation Center, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China.
Shuai YuanEchocardiography and Vascular Ultrasound Center, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China.
Han ZhangDepartment of Cardiology and Atrial Fibrillation Center, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China.
Jianqiang ZhaoDepartment of Cardiology, The Fourth Affiliated Hospital, College of Medicine, Zhejiang University, Yiwu, China.
Liangrong ZhengDepartment of Cardiology and Atrial Fibrillation Center, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China.ORCID 0000-0002-3998-1999
First Affiliated Hospital Zhejiang University · CNTaizhou Central Hospital · CNThe Fourth People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prolonged pathological myocardial hypertrophy leads to end-stage heart failure. Thymoquinone (TQ), a bioactive component extracted from Nigella sativa seeds, is extensively used in ethnomedicine to treat a broad spectrum of disorders. However, it remains unclear whether TQ protects the heart from pathological hypertrophy. This study was conducted to examine the potential utility of TQ for treatment of pathological cardiac hypertrophy and if so, to elucidate the underlying mechanisms. Male C57BL/6J mice underwent either transverse aortic constriction (TAC) or sham operation, followed by TQ treatment for six consecutive weeks. In vitro experiments consisted of neonatal rat cardiomyocytes (NRCMs) that were exposed to phenylephrine (PE) stimulation to induce cardiomyocyte hypertrophy. In this study, we observed that systemic administration of TQ preserved cardiac contractile function, and alleviated cardiac hypertrophy, fibrosis and oxidative stress in TAC-challenged mice. The in vitro experiments showed that TQ treatment attenuated the PE-induced hypertrophic response in NRCMs. Mechanistical experiments showed that supplementation of TQ induced reactivation of the AMP-activated protein kinase (AMPK) with concomitant inhibition of ERK 1/2, p38 and JNK1/2 MAPK cascades. Furthermore, we demonstrated that compound C, an AMPK inhibitor, abolished the protective effects of TQ in in vivo and in vitro experiments. Altogether, our study disclosed that TQ provides protection against myocardial hypertrophy in an AMPK-dependent manner and identified it as a promising agent for the treatment of myocardial hypertrophy.

Indexed as

AMP-Activated Protein KinasesCardiomegalyAnimalsBenzoquinonesMaleMiceMice, Inbred C57BLMyocytes, CardiacRatsAMP-Activated Protein KinasesBenzoquinonesthymoquinoneAMPKcardiac hypertrophyfibrosisheart failureoxidative stressthymoquinone

Identifiers

PMID34953026
PMCPMC8817125
OpenAlexW4200299924

What OpenQuestion holds

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LicenceCC BY
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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.