Evidence map›Paper›PMID 32444995›Full record

ArticleCardiovascular drugs and therapy2020

Protection of Sacubitril/Valsartan against Pathological Cardiac Remodeling by Inhibiting the NLRP3 Inflammasome after Relief of Pressure Overload in Mice.

Xueling Li, Qin Zhu, Qingcheng Wang, Qinggang Zhang, Yaru Zheng, Lihong Wang, Qinyang Jin

Open access · hybridAbstract read
In one paragraph

Article in Cardiovascular drugs and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing 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

21 citing papers in PubMed, 36 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.

Xueling LiDepartment of Cardiology, Zhejiang provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou, 310014, China.ORCID 0000-0003-3975-6860
Qin ZhuDepartment of Nephrology, Hangzhou Hospital of Traditional Chinese Medicine, Hangzhou, China.
Qingcheng WangDepartment of Cardiology, Hangzhou Yuhang Hospital of Traditional Chinese Medicine, Hangzhou, China.
Qinggang ZhangDepartment of Cardiology, Zhejiang provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou, 310014, China.
Yaru ZhengDepartment of Cardiology, Zhejiang provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou, 310014, China.
Lihong WangDepartment of Cardiology, Zhejiang provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou, 310014, China. zryxnk@163.com.
Qinyang JinDepartment of Cardiology, Zhejiang provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou, 310014, China. jqy119@163.com.
Hangzhou Medical College · CNHangzhou Hospital of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

aimsThe persistent existence of pathological cardiac remodeling, resulting from aortic stenosis, is related to poor clinical prognosis after successful transcatheter aortic valve replacement (TAVR). Sacubitril/valsartan (Sac/Val), comprising an angiotensin receptor blocker and a neprilysin inhibitor, has been demonstrated to have a beneficial effect against pathological cardiac remodeling, including cardiac fibrosis and inflammation in heart failure. The aim of this study was to determine whether Sac/Val exerts a cardioprotective effect after pressure unloading in mice. METHODS AND

resultsMale C57BL/6 J mice were subjected to debanding (DB) surgery after 8 weeks (wk) of aortic banding (AB). Cardiac function was assessed by echocardiography, which indicated a protective effect of Sac/Val after DB. After treatment with Sac/Val post DB, decreased heart weight and myocardial cell size were observed in mouse hearts. In addition, histological analysis, immunofluorescence, and western blot results showed that Sac/Val attenuated cardiac fibrosis and inflammation after DB. Finally, our data indicated that Sac/Val treatment could significantly suppress NF-κB signaling and NLRP3 inflammasome activation in mice after relief of pressure overload.

conclusionSac/Val exerted its beneficial effects to prevent maladaptive cardiac fibrosis and dysfunction in mice following pressure unloading, which was at least partly due to the inhibition of NLRP3 inflammasome activation.

Indexed as

AminobutyratesAngiotensin II Type 1 Receptor BlockersAnimalsBiphenyl CompoundsDisease Models, AnimalDrug CombinationsFibrosisHypertrophy, Left VentricularInflammasomesMaleMice, Inbred C57BLMyocardiumNeprilysinNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinProtease InhibitorsAminobutyratesAngiotensin II Type 1 Receptor BlockersBiphenyl CompoundsDrug CombinationsInflammasomesNeprilysinNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseProtease Inhibitorssacubitril and valsartan sodium hydrate drug combinationTetrazolesValsartanCardiac remodelingNLRP3 inflammasomePressure unloadingSacubitril/valsartan

Identifiers

PMID32444995
PMCPMC7497317
OpenAlexW3028321329

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.