Evidence map›Paper›PMID 37289363›Full record

ArticleMolecular biology reports2023

Synergistic effect of elevated glucose levels with SARS-CoV-2 spike protein induced NOX-dependent ROS production in endothelial cells.

Jiahao Zhang, Li He, Rong Huang, Juan Felipe Alvarez, David H Yang, Qihao Sun, Fengqin Wang, Zhiyong Peng, Nanhui Jiang, Lianjiu Su

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

Article in Molecular biology reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

11 citing papers in PubMed, 11 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

10 authors at 2 institutions in 2 countries.

Jiahao Zhang *Department of Critical Care Medicine, Zhongnan Hospital of Wuhan University, Hubei Province, Wuhan 430071, China.
Li He *Department of Critical Care Medicine, Zhongnan Hospital of Wuhan University, Hubei Province, Wuhan 430071, China.
Rong Huang *Department of Critical Care Medicine, Zhongnan Hospital of Wuhan University, Hubei Province, Wuhan 430071, China.
Juan Felipe AlvarezDivision of Cardiology, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA, USA.
David H YangDivision of Cardiology, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA, USA.
Qihao SunDivision of Cardiology, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA, USA.
Fengqin WangDepartment of Critical Care Medicine, Zhongnan Hospital of Wuhan University, Hubei Province, Wuhan 430071, China.
Zhiyong PengDepartment of Critical Care Medicine, Zhongnan Hospital of Wuhan University, Hubei Province, Wuhan 430071, China.
Nanhui JiangDepartment of Critical Care Medicine, Zhongnan Hospital of Wuhan University, Hubei Province, Wuhan 430071, China. 2014302180012@whu.edu.cn.
Lianjiu SuDepartment of Critical Care Medicine, Zhongnan Hospital of Wuhan University, Hubei Province, Wuhan 430071, China. sulianjiu@whu.edu.cn.ORCID http://orcid.org/0000-0001-6822-6602
Wuhan University · CNUniversity of California, Los Angeles · US

Funding

Innovation Cultivation Foundation of Wuhan University/Zhongnan Hospital 413000345/CXPY2020017National Natural Science Foundation of China 82102298Research Project Foundation of Zhongnan Hospital ZNYB2020013
6 · The paper itself

Abstract

backgroundDiabetic patients infected with coronavirus disease 2019 (COVID-19) often have a higher probability of organ failure and mortality. The potential cellular mechanisms through which blood glucose exacerbates tissue damage due to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is still unclear. METHODS AND

resultsWe cultured endothelial cells within differing glucose mediums with an increasing concentration gradient of SARS-CoV-2 Spike protein (S protein). S protein can cause the reduction of ACE2 and TMPRSS2, and activation of NOX2 and NOX4. A high glucose medium was shown to aggravate the decrease of ACE2 and activation of NOX2 and NOX4 in cultured cells, but had no effect on TMPRSS2. S protein mediated activation of the ACE2-NOX axis induced oxidative stress and apoptosis within endothelial cells, leading to cellular dysfunction via the reduction of NO and tight junction proteins which may collectively be exacerbated by elevated glucose. In addition, the glucose variability model demonstrated activation of the ACE2-NOX axis in a similar manner observed in the high glucose model in vitro.

conclusionsOur present study provides evidence for a mechanism through which hyperglycemia aggravates endothelial cell injury resulting from S protein mediated activation of the ACE2-NOX axis. Our research thus highlights the importance of strict monitoring and control of blood glucose levels within the context of COVID-19 treatment to potentially improve clinical outcomes.

Indexed as

COVID-19Angiotensin-Converting Enzyme 2Blood GlucoseCOVID-19 Drug TreatmentEndothelial CellsHumansPeptidyl-Dipeptidase AReactive Oxygen SpeciesSARS-CoV-2Spike Glycoprotein, CoronavirusAngiotensin-Converting Enzyme 2Blood GlucosePeptidyl-Dipeptidase AReactive Oxygen SpeciesSpike Glycoprotein, Coronavirusspike protein, SARS-CoV-2ACE2COVID-19Endothelial cellsHigh glucoseNOXsROSS protein

Identifiers

PMID37289363
PMCPMC10249571
OpenAlexW4379769442

What OpenQuestion holds

Textmetadata
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.