Evidence map›Paper›PMID 33014281›Full record

ArticleOxidative medicine and cellular longevity2020

LCZ696 Ameliorates Oxidative Stress and Pressure Overload-Induced Pathological Cardiac Remodeling by Regulating the Sirt3/MnSOD Pathway.

Shi Peng, Xiao-Feng Lu, Yi-Ding Qi, Jing Li, Juan Xu, Tian-You Yuan, Xiao-Yu Wu, Yu Ding, Wen-Hua Li, Gen-Qing Zhou and 4 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oxidative medicine and cellular longevity, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

30 citing papers in PubMed, 44 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

14 authors at 2 institutions in 1 country.

Shi PengDepartment of Cardiology, Shanghai General Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.ORCID https://orcid.org/0000-0001-7842-9892
Xiao-Feng LuDepartment of Cardiology, Shanghai General Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Yi-Ding QiDepartment of Cardiology, Shanghai Chest Hospital, Shanghai Jiao Tong University, China.
Jing LiDepartment of Ultrasound, The Second Affiliated Hospital of Soochow University, Suzhou, China.
Juan XuDepartment of Cardiology, Shanghai General Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Tian-You YuanDepartment of Cardiology, Shanghai General Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Xiao-Yu WuDepartment of Cardiology, Shanghai General Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Yu DingDepartment of Cardiology, Shanghai General Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Wen-Hua LiDepartment of Cardiology, Affiliated Wujin Hospital of Jiangsu University, China.
Gen-Qing ZhouDepartment of Cardiology, Shanghai General Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Yong WeiDepartment of Cardiology, Shanghai General Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Jun LiDepartment of Cardiology, Shanghai General Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Song-Wen ChenDepartment of Cardiology, Shanghai General Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.ORCID https://orcid.org/0000-0002-6492-5702
Shao-Wen LiuDepartment of Cardiology, Shanghai General Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.ORCID https://orcid.org/0000-0002-0351-6868
Shanghai Jiao Tong University · CNJiangsu University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsWe aimed to investigate whether LCZ696 protects against pathological cardiac hypertrophy by regulating the Sirt3/MnSOD pathway.

methods

resultsPathological hypertrophic stimuli caused cardiac hypertrophy and fibrosis and reduced the expression levels of Sirt3 and MnSOD. LCZ696 alleviated the accumulation of oxidative reactive oxygen species (ROS) and cardiomyocyte apoptosis. Furthermore, Sirt3 deficiency abolished the protective effect of LCZ696 on cardiomyocyte hypertrophy, indicating that LCZ696 induced the upregulation of MnSOD and phosphorylation of AMPK through a Sirt3-dependent pathway.

conclusionsLCZ696 may mitigate myocardium oxidative stress and apoptosis in pressure overload-induced heart failure by regulating the Sirt3/MnSOD pathway.

Indexed as

AminobutyratesAMP-Activated Protein KinasesAnimalsApoptosisBiphenyl CompoundsCardiomegalyDrug CombinationsMaleMiceMice, Inbred C57BLMyocardiumMyocytes, CardiacOxidative StressProto-Oncogene Proteins c-bcl-2Reactive Oxygen SpeciesRNA InterferenceAminobutyratesAMP-Activated Protein KinasesBiphenyl CompoundsDrug CombinationsProto-Oncogene Proteins c-bcl-2Reactive Oxygen SpeciesRNA, Small Interferingsacubitril and valsartan sodium hydrate drug combinationSirtuin 3Superoxide DismutaseTetrazolesValsartan

Identifiers

PMID33014281
PMCPMC7519988
OpenAlexW3087594112

What OpenQuestion holds

Textmetadata
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.