Evidence map›Paper›PMID 36585107›Full record

ArticleJournal of advanced research2023

iNOS contributes to heart failure with preserved ejection fraction through mitochondrial dysfunction and Akt S-nitrosylation.

Yongzheng Guo, Junjie Wen, An He, Can Qu, Yuce Peng, Suxin Luo, Xiaowen Wang

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

Article in Journal of advanced research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
5.2field-weighted citation impact, top 3% 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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 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.

Yongzheng GuoDivision of Cardiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.
Junjie WenDivision of Cardiology, West China Guang'an Hospital of Sichan University, Guang'an 638500, China.
An HeDivision of Cardiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.
Can QuDepartment of Pharmacy, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.
Yuce PengDivision of Cardiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.
Suxin LuoDivision of Cardiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China. Electronic address: luosuxin@hospital.cqmu.edu.cn.
Xiaowen WangDepartment of Cardiothoracic Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China. Electronic address: xiaowenwang@cqmu.edu.cn.
Chongqing Medical University · CNFirst Affiliated Hospital of Chongqing Medical University · CNGuang’anmen Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionDespite the high morbidity and mortality of heart failure with preserved fraction (HFpEF), there are currently no effective therapies for this condition. Moreover, the pathophysiological basis of HFpEF remains poorly understood.

objectiveThe aim of the present study was to investigate the role of inducible nitric oxide synthase (iNOS) and its underlying mechanism in a high-fat diet and N

methodsThe selective iNOS inhibitor L-NIL was used to examine the effects of short-term iNOS inhibition, whereas the long-term effects of iNOS deficiency were evaluated using iNOS-null mice. Cardiac and mitochondrial function, oxidative stress and Akt S-nitrosylation were then measured.

resultsThe results demonstrated that both pharmacological inhibition and iNOS knockout mitigated mitochondrial dysfunction, oxidative stress and Akt S-nitrosylation, leading to an ameliorated HFpEF phenotype in mice. In vitro, iNOS directly induced Akt S-nitrosylation at cysteine 224 residues , leading to oxidative stress, while inhibiting insulin-mediated glucose uptake in myocytes.

conclusionAltogether, the present findings suggested an important role for iNOS in the pathophysiological development of HFpEF, indicating that iNOS inhibition may represent a potential therapeutic strategy for HFpEF.

Indexed as

Heart FailureMitochondriaNitric Oxide Synthase Type IIProto-Oncogene Proteins c-aktAnimalsLysineMiceOxidative StressStroke VolumeLysineN(6)-(1-iminoethyl)lysineNitric Oxide Synthase Type IIProto-Oncogene Proteins c-aktAkt S-nitrosylationHFpEFiNOSMitochondrial function

Identifiers

PMID36585107
PMCPMC9811328
OpenAlexW4220879846

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.