Evidence map›Paper›PMID 36332749›Full record

ArticleInternational journal of cardiology2023

NOX2 and NOX5 are increased in cardiac microvascular endothelium of deceased COVID-19 patients.

Zhu Jiang, Linghe Wu, Britt van der Leeden, Albert C van Rossum, Hans W M Niessen, Paul A J Krijnen

Open access · hybridAbstract read
In one paragraph

Article in International journal of cardiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.1field-weighted citation impact, top 21% 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

10 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
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  8. Cross-Talk of NADPH Oxidases and Inflammation in Obesity.Antioxidants (Basel, Switzerland) · 2023
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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 2 institutions in 1 country.

Zhu JiangDepartment of Pathology, Amsterdam UMC Location Vrije Universiteit Amsterdam, Pathology, De Boelelaan 1117, Amsterdam, the Netherlands; Amsterdam Cardiovascular Sciences, Microcirculation, Amsterdam, the Netherlands. Electronic address: z.jiang@amsterdamumc.nl.
Linghe WuDepartment of Pathology, Amsterdam UMC Location Vrije Universiteit Amsterdam, Pathology, De Boelelaan 1117, Amsterdam, the Netherlands; Amsterdam Cardiovascular Sciences, Microcirculation, Amsterdam, the Netherlands.
Britt van der LeedenDepartment of Pathology, Amsterdam UMC Location Vrije Universiteit Amsterdam, Pathology, De Boelelaan 1117, Amsterdam, the Netherlands; Amsterdam Institute for Infection and Immunity, AUMC, Location VUmc, Amsterdam, the Netherlands.
Albert C van RossumAmsterdam Cardiovascular Sciences, Microcirculation, Amsterdam, the Netherlands; Department of Cardiology, AUMC, location VUmc, Amsterdam, the Netherlands.
Hans W M NiessenDepartment of Pathology, Amsterdam UMC Location Vrije Universiteit Amsterdam, Pathology, De Boelelaan 1117, Amsterdam, the Netherlands; Amsterdam Cardiovascular Sciences, Microcirculation, Amsterdam, the Netherlands; Department of Cardiac Surgery, AUMC, Location AMC and VUmc, Amsterdam, the Netherlands.
Paul A J KrijnenDepartment of Pathology, Amsterdam UMC Location Vrije Universiteit Amsterdam, Pathology, De Boelelaan 1117, Amsterdam, the Netherlands; Amsterdam Cardiovascular Sciences, Microcirculation, Amsterdam, the Netherlands.
Amsterdam Neuroscience · NLAmsterdam University Medical Centers · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCardiac injury and inflammation are common findings in COVID-19 patients. Autopsy studies have revealed cardiac microvascular endothelial damage and thrombosis in COVID-19 patients, indicative of microvascular dysfunction in which reactive oxygen species (ROS) may play a role. We explored whether the ROS producing proteins NOX2, NOX4 and NOX5 are involved in COVID-19-induced cardio-microvascular endothelial dysfunction.

methodsHeart tissue were taken from the left (LV) and right (RV) ventricle of COVID-19 patients (n = 15) and the LV of controls (n = 14) at autopsy. The NOX2-, NOX4-, NOX5- and Nitrotyrosine (NT)-positive intramyocardial blood vessels fractions were quantitatively analyzed using immunohistochemistry.

resultsThe LV NOX2+, NOX5+ and NT+ blood vessels fractions in COVID-19 patients were significantly higher than in controls. The fraction of NOX4+ blood vessels in COVID-19 patients was comparable with controls. In COVID-19 patients, the fractions of NOX2+, NOX5+ and NT+ vessels did not differ significantly between the LV and RV, and correlated positively between LV and RV in case of NOX5 (r = 0.710; p = 0.006). A negative correlation between NOX5 and NOX2 (r = -0.591; p = 0.029) and between NOX5 and disease time (r = -0.576; p = 0.034) was noted in the LV of COVID-19 patients.

conclusionWe show the induction of NOX2 and NOX5 in the cardiac microvascular endothelium in COVID-19 patients, which may contribute to the previously observed cardio-microvascular dysfunction in COVID-19 patients. The exact roles of these NOXes in pathogenesis of COVID-19 however remain to be elucidated.

Indexed as

COVID-19NADPH Oxidase 2NADPH Oxidase 5Endothelium, VascularHeartHumansReactive Oxygen SpeciesCYBB protein, humanNADPH Oxidase 2NADPH Oxidase 5NOX5 protein, humanReactive Oxygen SpeciesCOVID-19HeartMicrovasculatureNOX2NOX5

Identifiers

PMID36332749
PMCPMC9625847
OpenAlexW4307828832

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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.