Evidence map›Paper›PMID 33519510›Full record

ReviewFrontiers in physiology2020

SARS-CoV-2 Mediated Endothelial Dysfunction: The Potential Role of Chronic Oxidative Stress.

Ryan Chang, Abrar Mamun, Abishai Dominic, Nhat-Tu Le

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed, 2 pooled it
11.7field-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

95 citing papers in PubMed, 2 syntheses or guidelines pooled it, 131 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Impact of COVID-19 Booster Vaccination on Serum Redox Homeostasis.International journal of molecular sciences · 2026
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35 more citing papers are in PubMed but not listed here.

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

4 authors at 4 institutions in 1 country.

Ryan ChangCollege of Arts & Sciences, Washington University in St. Louis, St. Louis, MO, United States.
Abrar MamunWiess School of Natural Sciences, Rice University, Houston, TX, United States.
Abishai DominicDepartment of Molecular and Cellular Medicine, College of Medicine, Texas A&M University, College Station, TX, United States.
Nhat-Tu LeDepartment of Cardiovascular Sciences, Center for Cardiovascular Regeneration, Houston Methodist Research Institute, Houston, TX, United States.
Houston Methodist · USRice University · USTexas A&M University · USWashington University in St. Louis · US

Funding

Pathological flow-induced endothelial damage and plaque erosionR01HL149303 · NHLBI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI ABE, JUN-ICHI, COOKE, JOHN P · 2019 to 2022
$3.2M
A Novel Role for MAGI1 in regulating non-canonical LATS signaling and atherosclerotic plaque formationR01HL134740 · NHLBI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LE, NHAT-TU · 2017 to 2021
$2.0M
NHLBI NIH HHS R01 HL134740NHLBI NIH HHS R01 HL149303
6 · The paper itself

Abstract

Endothelial cells have emerged as key players in SARS-CoV-2 infection and COVID-19 inflammatory pathologies. Dysfunctional endothelial cells can promote chronic inflammation and disease processes like thrombosis, atherosclerosis, and lung injury. In endothelial cells, mitochondria regulate these inflammatory pathways via redox signaling, which is primarily achieved through mitochondrial reactive oxygen species (mtROS). Excess mtROS causes oxidative stress that can initiate and exacerbate senescence, a state that promotes inflammation and chronic endothelial dysfunction. Oxidative stress can also activate feedback loops that perpetuate mitochondrial dysfunction, mtROS overproduction, and inflammation. In this review, we provide an overview of phenotypes mediated by mtROS in endothelial cells - such as mitochondrial dysfunction, inflammation, and senescence - as well as how these chronic states may be initiated by SARS-CoV-2 infection of endothelial cells. We also propose that SARS-CoV-2 activates mtROS-mediated feedback loops that cause long-term changes in host redox status and endothelial function, promoting cardiovascular disease and lung injury after recovery from COVID-19. Finally, we discuss the implications of these proposed pathways on long-term vascular health and potential treatments to address these chronic conditions.

Indexed as

CardiovascularEndMTendothelial cellsinflammationmitochondrial dysfunctionoxidative stressSARS-CoV-2senescence

Identifiers

PMID33519510
PMCPMC7844210
OpenAlexW3124849444

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.