Evidence map›Paper›PMID 36829885›Full record

ArticleAntioxidants (Basel, Switzerland)2023

COVID-19 Causes Ferroptosis and Oxidative Stress in Human Endothelial Cells.

Stanislovas S Jankauskas, Urna Kansakar, Celestino Sardu, Fahimeh Varzideh, Roberta Avvisato, Xujun Wang, Alessandro Matarese, Raffaele Marfella, Marcello Ziosi, Jessica Gambardella and 1 more

Open access · goldAbstract read
In one paragraph

Article in Antioxidants (Basel, Switzerland), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
19.8field-weighted citation impact, top 1% 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

49 citing papers in PubMed, 1 synthesis or guideline pooled it, 84 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

11 authors at 4 institutions in 2 countries.

Stanislovas S JankauskasDepartment of Medicine, Division of Cardiology, Wilf Family Cardiovascular Research Institute, Einstein Institute for Aging Research, Albert Einstein College of Medicine, New York, NY 10461, USA.ORCID 0000-0002-0843-5098
Urna KansakarDepartment of Medicine, Division of Cardiology, Wilf Family Cardiovascular Research Institute, Einstein Institute for Aging Research, Albert Einstein College of Medicine, New York, NY 10461, USA.
Celestino SarduUniversity of Campania "Luigi Vanvitelli", 81100 Caserta, Italy.ORCID 0000-0001-5099-3790
Fahimeh VarzidehDepartment of Medicine, Division of Cardiology, Wilf Family Cardiovascular Research Institute, Einstein Institute for Aging Research, Albert Einstein College of Medicine, New York, NY 10461, USA.
Roberta AvvisatoDepartment of Medicine, Division of Cardiology, Wilf Family Cardiovascular Research Institute, Einstein Institute for Aging Research, Albert Einstein College of Medicine, New York, NY 10461, USA.
Xujun WangDepartment of Medicine, Division of Cardiology, Wilf Family Cardiovascular Research Institute, Einstein Institute for Aging Research, Albert Einstein College of Medicine, New York, NY 10461, USA.
Alessandro MatareseCardarelli Hospital, 80131 Naples, Italy.
Raffaele MarfellaUniversity of Campania "Luigi Vanvitelli", 81100 Caserta, Italy.ORCID 0000-0003-3960-9270
Marcello ZiosiNew York Genome Center, New York, NY 10013, USA.
Jessica GambardellaDepartment of Medicine, Division of Cardiology, Wilf Family Cardiovascular Research Institute, Einstein Institute for Aging Research, Albert Einstein College of Medicine, New York, NY 10461, USA.
Gaetano SantulliDepartment of Medicine, Division of Cardiology, Wilf Family Cardiovascular Research Institute, Einstein Institute for Aging Research, Albert Einstein College of Medicine, New York, NY 10461, USA.ORCID 0000-0001-7231-375X
Albert Einstein College of Medicine · USUniversity of Campania "Luigi Vanvitelli" · ITFatebenefratelli Hospital · ITNew York Genome Center · US

Funding

CTSA Administrative Supplement for Informatics Core: A novel AI/ML system to predict respiratory failure and ARDS in Covid-19 patientsUL1TR002556 · NCATS · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI KELLER, MARLA J, KIM, MIMI Y · 2018 to 2022
$26.7M
REGULATION OF THE INSULIN RECEPTOR KINASER01DK033823 · NIDDK · UNIVERSITY OF IOWA · PI KURLAND, IRWIN JACK, PESSIN, JEFFREY E. · 1986 to 2022
$6.7M
Modulation of Mitofusin Activity to Treat Heart DiseaseR01HL159062 · NHLBI · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI KITSIS, RICHARD N · 2021 to 2024
$2.6M
Caspase-9 as a nodal point connecting necrotic and apoptotic cell death in myocardial infarctionR01HL164772 · NHLBI · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI KITSIS, RICHARD N · 2022 to 2025
$2.5M
Functional role of IP3 receptors in the regulation of cardiac myofibroblastsR01HL146691 · NHLBI · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI SANTULLI, GAETANO · 2019 to 2023
$2.1M
Mechanisms of cardiovascular diseaseT32HL144456 · NHLBI · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI Carlos Jose Rodriguez, Nicholas E Sibinga · 2019 to 2026
$1.9M
Beta Cell Intracellular Calcium and DiabetesR01DK123259 · NIDDK · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI SANTULLI, GAETANO · 2020 to 2023
$1.7M
NCATS NIH HHS UL1 TR002556NHLBI NIH HHS R01 HL146691NHLBI NIH HHS R01 HL159062NHLBI NIH HHS R01 HL164772NHLBI NIH HHS T32 HL144456NIDDK NIH HHS R01 DK033823NIDDK NIH HHS R01 DK123259
6 · The paper itself

Abstract

Oxidative stress and endothelial dysfunction have been shown to play crucial roles in the pathophysiology of COVID-19 (coronavirus disease 2019). On these grounds, we sought to investigate the impact of COVID-19 on lipid peroxidation and ferroptosis in human endothelial cells. We hypothesized that oxidative stress and lipid peroxidation induced by COVID-19 in endothelial cells could be linked to the disease outcome. Thus, we collected serum from COVID-19 patients on hospital admission, and we incubated these sera with human endothelial cells, comparing the effects on the generation of reactive oxygen species (ROS) and lipid peroxidation between patients who survived and patients who did not survive. We found that the serum from non-survivors significantly increased lipid peroxidation. Moreover, serum from non-survivors markedly regulated the expression levels of the main markers of ferroptosis, including GPX4, SLC7A11, FTH1, and SAT1, a response that was rescued by silencing TNFR1 on endothelial cells. Taken together, our data indicate that serum from patients who did not survive COVID-19 triggers lipid peroxidation in human endothelial cells.

Indexed as

COVID-19endothelial dysfunctionferroptosisHUVECinflammationlipid peroxidationlong COVIDoxidative stressoxytosisperoxidationROSSARS-CoV-2

Identifiers

PMID36829885
PMCPMC9952002
OpenAlexW4318705692

What OpenQuestion holds

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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.