Evidence map›Paper›PMID 34759275›Full record

ArticleCell death & disease2021

Circ-SIRT1 inhibits cardiac hypertrophy via activating SIRT1 to promote autophagy.

Weichen Wang, Longlong Wang, Mengyue Yang, Chunwei Wu, Rui Lan, Weiwei Wang, Yuze Li

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.3field-weighted citation impact, top 6% 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

33 citing papers in PubMed, 52 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 2 institutions in 1 country.

Weichen WangDepartment of Cardiology, the First Hospital of China Medical University, 110001, Shenyang, Liaoning, People's Republic of China.
Longlong WangDepartment of Cardiology, the First Hospital of China Medical University, 110001, Shenyang, Liaoning, People's Republic of China.
Mengyue YangDepartment of Cardiology, the First Hospital of China Medical University, 110001, Shenyang, Liaoning, People's Republic of China.
Chunwei WuDepartment of Cardiology, the First Hospital of China Medical University, 110001, Shenyang, Liaoning, People's Republic of China.
Rui LanDepartment of Cardiology, the First Hospital of China Medical University, 110001, Shenyang, Liaoning, People's Republic of China.
Weiwei WangDepartment of Cardiology, the First Hospital of China Medical University, 110001, Shenyang, Liaoning, People's Republic of China.
Yuze LiDepartment of Cardiology, the First Hospital of China Medical University, 110001, Shenyang, Liaoning, People's Republic of China. jrhs@163.com.
China Medical University · CNFirst Hospital of China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mounting studies have substantiated that abrogating autophagy contributes to cardiac hypertrophy (CH). Sirtuin 1 (SIRT1) has been reported to support autophagy and inhibit CH. However, the upstream regulation mechanism behind the regulation of SIRT1 level in CH remains unclear. Circular RNAs (circRNAs) are vital modulators in diverse human diseases including CH. This study intended to investigate the regulatory mechanism of circRNA on SIRT1 expression in CH. CH model was established by angiotensin II (Ang II) fusion or transverse aortic constriction (TAC) surgery and Ang II treatment on hiPSC-CMs and H9c2 cells in vitro. Our results showed that circ-SIRT1 (hsa_circ_0093884) expression was downregulated in Ang II-treated hiPSC-CMs, and confirmed that its conserved mouse homolog circ-Sirt1 (mmu_circ_0002354) was expressed at low levels in Ang II-treated H9c2 cells and TAC-induced mice model. Functionally, circ-SIRT1/circ-Sirt1 attenuated Ang II-induced CH and induced autophagy in hiPSC-CMs and H9c2 cardiomyocytes. Mechanistically, circ-SIRT1 could upregulate its host gene SIRT1 at the post-transcriptional level by sponging miR-3681-3p/miR-5195-3p and stabilized SIRT1 protein at the post-translational level by recruiting USP22 to induce deubiquitination on SIRT1 protein. Further, SIRT1 knockdown could rescue the effect of circ-SIRT1 upregulation on Ang II-induced CH and autophagy in vitro and in vivo. In conclusion, we first uncovered that circ-SIRT1 restrains CH via activating SIRT1 to promote autophagy, indicating circ-SIRT1 as a promising target to alleviate CH.

Indexed as

AnimalsAutophagyCardiomegalyDisease Models, AnimalHumansMiceRNA, CircularSirtuin 1TransfectionUp-RegulationRNA, CircularSirtuin 1

Identifiers

PMID34759275
PMCPMC8580993
OpenAlexW3214092507

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.