Evidence map›Paper›PMID 36840500›Full record

ArticleImmunity, inflammation and disease2023

PON2 ameliorates Ang II-induced cardiomyocyte injury by targeting the CANX/NOX4 signaling pathway.

Yuanzheng Ye, Jian Zhang, Yankai Guo, Jiajun Zhu, Baopeng Tang, Ping Fan

Open access · goldAbstract read
In one paragraph

Article in Immunity, inflammation and disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

6 citing papers in PubMed, 14 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

6 authors at 1 institution in 1 country.

Yuanzheng YeDepartment of Cardiac Function, State Key Laboratory of Pathogenesis Prevention and Treatment of High Incidence Diseases in Central Asia, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, China.
Jian ZhangCardiact Care Unit, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, China.
Yankai GuoXinjiang Key Laboratory of Cardiac Electrophysiology and Cardiac Remodeling, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, China.
Jiajun ZhuCardiact Care Unit, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, China.
Baopeng TangXinjiang Key Laboratory of Cardiac Electrophysiology and Cardiac Remodeling, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, China.
Ping FanDepartment of Cardiac Function, State Key Laboratory of Pathogenesis Prevention and Treatment of High Incidence Diseases in Central Asia, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, China.ORCID 0000-0001-5857-8217
Xinjiang Medical University · CN

Funding

Regional Collaborative Innovation Project (Science and Technology Assistance Plan for Xinjiang) 2022E02111State Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia Fund SKL-HIDCA-2020-7
6 · The paper itself

Abstract

backgroundThe incidence of heart failure (HF) presents an escalating trend annually, second only to cancer. Few literatures are available regarding on the role of paraoxonase 2 (PON2) in HF so far despite the protective role of PON2 in cardiovascular diseases.

methodsPON2 expression in AC16 cells was examined with reverse transcriptase-quantitative polymerase chain reaction and western blot following angiotensin II (Ang II) challenging. After PON2 elevation, 2, 7-dichlorofluorescein diacetate assay estimated reactive oxygen species content, related kits appraised oxidative stress, enzyme-linked immunosorbent assay evaluated inflammatory levels, and Western blot was applied to the analysis of apoptosis levels. Research on cytoskeleton was conducted by immunofluorescence (IF), and Western blot analysis of the expressions of hypertrophy-related proteins was performed. BioGRID and GeneMania databases were used to analyze the relationship between PON2 and Calnexin (CANX), which was corroborated by co-immunoprecipitation experiment. Subsequently, PON2 and CANX were simultaneously overexpressed in AC16 cells induced by Ang II to further figure out the mechanism.

resultsPON2 expression was depleted in Ang II-induced AC16 cells. PON2 might mediate CANX/NOX4 signaling to inhibit oxidation, inflammatory, hypertrophy, and damage in Ang II-induced AC16 cells.

conclusionPON2 can ease Ang II-induced cardiomyocyte injury via targeting CANX/NOX4 signaling.

Indexed as

Angiotensin IIAryldialkylphosphataseCalnexinMyocytes, CardiacNADPH Oxidase 4HumansHypertrophySignal TransductionAngiotensin IIAryldialkylphosphataseCalnexinCANX protein, humanNADPH Oxidase 4NOX4 protein, humanPON2 protein, humanAng II-induced cardiomyocyte injuryCANX/NOX4 signaling pathwayheart failurePON2

Identifiers

PMID36840500
PMCPMC9910164
OpenAlexW4319787564

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.