Evidence map›Paper›PMID 28333148›Full record

ArticleCell death & disease2017

Salusin-β contributes to oxidative stress and inflammation in diabetic cardiomyopathy.

Ming-Xia Zhao, Bing Zhou, Li Ling, Xiao-Qing Xiong, Feng Zhang, Qi Chen, Yue-Hua Li, Yu-Ming Kang, Guo-Qing Zhu

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
9.2field-weighted citation impact, top 2% 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

51 citing papers in PubMed, 95 citations in OpenAlex.

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  10. Research progress on intranasal treatment for Parkinson's disease.Neuroprotection (Chichester, England) · 2024
    Review
  11. Article
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  14. Serum salusin-α and -β levels in patients with parkinson's disease.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2024
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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

9 authors at 2 institutions in 1 country.

Ming-Xia ZhaoDepartment of Physiology, Key Laboratory of Cardiovascular Disease and Molecular Intervention, Nanjing Medical University, Nanjing, China.
Bing ZhouDepartment of Physiology, Key Laboratory of Cardiovascular Disease and Molecular Intervention, Nanjing Medical University, Nanjing, China.
Li LingDepartment of Physiology, Key Laboratory of Cardiovascular Disease and Molecular Intervention, Nanjing Medical University, Nanjing, China.
Xiao-Qing XiongDepartment of Physiology, Key Laboratory of Cardiovascular Disease and Molecular Intervention, Nanjing Medical University, Nanjing, China.
Feng ZhangDepartment of Physiology, Key Laboratory of Cardiovascular Disease and Molecular Intervention, Nanjing Medical University, Nanjing, China.
Qi ChenDepartment of Pathophysiology, Nanjing Medical University, Nanjing, China.
Yue-Hua LiDepartment of Pathophysiology, Nanjing Medical University, Nanjing, China.
Yu-Ming KangDepartment of Physiology and Pathophysiology, Cardiovascular Research Center, Xi'an Jiaotong University School of Medicine, Xi'an, China.
Guo-Qing ZhuDepartment of Physiology, Key Laboratory of Cardiovascular Disease and Molecular Intervention, Nanjing Medical University, Nanjing, China.ORCID 0000-0002-3132-9592
Nanjing Medical University · CNXi'an Jiaotong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Salusin-β accelerates inflammatory responses in vascular endothelial cells, and increases oxidative stress in vascular smooth muscle cells. Plasma salusin-β levels were increased in diabetic patients. This study was designed to determine whether salusin-β is involved in the pathogenesis of diabetic cardiomyopathy (DCM), and whether knockdown of salusin-β attenuates cardiac inflammation and oxidative stress in rats with DCM. H9c2 or neonatal rat cardiomyocytes were incubated with 33.3 mM of glucose to mimic the high glucose (HG) in diabetes. Streptozotocin and high-fat diet were used to induce type 2 diabetes in rats. HG induced salusin-β expression in H9c2 cells. Salusin-β caused greater responses of oxidative stress, NFκB activation and inflammation in HG-treated H9c2 cells than these in control H9c2 cells. Diphenyleneiodonium (a NAD(P)H oxidase inhibitor) or N-acetylcysteine (an antioxidant) inhibited the salusin-β-induced NFκB activation and inflammation. Bay11-7082 (a NFκB inhibitor) attenuated salusin-β-induced inflammation but not oxidative stress. Knockdown of salusin-β prevented the HG-induced oxidative stress, NFκB activation and inflammation in neonatal rat cardiomyocytes. Silencing salusin-β with adenoviruse-mediated shRNA had no significant effects on blood glucose and insulin resistance, but attenuated ventricular dysfunction in diabetic rats. Oxidative stress, NFκB activation, inflammation, salusin-β upregulation in myocardium of diabetic rats were prevented by knockdown of salusin-β. These results indicate that salusin-β contributes to inflammation in DCM via NOX2/ROS/NFκB signaling, and that knockdown of salusin-β attenuates cardiac dysfunction, oxidative stress and inflammation in DCM.

Indexed as

AnimalsBlood GlucoseCells, CulturedDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 2Diabetic CardiomyopathiesDiet, High-FatGene Expression RegulationInflammationInsulin ResistanceIntercellular Signaling Peptides and ProteinsMaleMyocytes, CardiacNF-kappa BOxidative StressRatsBlood GlucoseIntercellular Signaling Peptides and ProteinsNF-kappa Bsalusin-beta, rat

Identifiers

PMID28333148
PMCPMC5386515
OpenAlexW2603126331

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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.