Evidence map›Paper›PMID 32536875›Full record

ReviewFrontiers in physiology2020

Oxidative Stress and Microvessel Barrier Dysfunction.

Pingnian He, M A Hassan Talukder, Feng Gao

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 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

44 citing papers in PubMed, 64 citations in OpenAlex.

  1. Review
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  12. Time Course of Structural, Functional, Complement Changes and Inflammatory Processes in a Sodium Iodate Rat Model of Geographic Atrophy.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  13. Review
  14. Role of shear stress-induced red blood cell released ATP in atherosclerosis.American journal of physiology. Heart and circulatory physiology · 2025
    Article
  15. Article
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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

3 authors at 1 institution in 1 country.

Pingnian HeDepartment of Cellular and Molecular Physiology, College of Medicine, The Pennsylvania State University, Hershey, PA, United States.
M A Hassan TalukderDepartment of Cellular and Molecular Physiology, College of Medicine, The Pennsylvania State University, Hershey, PA, United States.
Feng GaoDepartment of Cellular and Molecular Physiology, College of Medicine, The Pennsylvania State University, Hershey, PA, United States.
Pennsylvania State University · US

Funding

Red blood cell released ATP in disturbed blood flow-initiated site specific vascular inflammation and atherosclerosisR01HL144620 · NHLBI · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI HE, PINGNIAN · 2019 to 2022
$3.1M
Nitric oxide and microvessel permeability in vivoR01HL130363 · NHLBI · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI HE, PINGNIAN · 2017 to 2020
$1.9M
Microparticles and microvascular dysfunction in diabetesR01DK097391 · NIDDK · WEST VIRGINIA UNIVERSITY · PI HE, PINGNIAN · 2013 to 2016
$1.4M
NHLBI NIH HHS R01 HL130363NHLBI NIH HHS R01 HL144620NIDDK NIH HHS R01 DK097391
6 · The paper itself

Abstract

Clinical and experimental evidence indicate that increased vascular permeability contributes to many disease-associated vascular complications. Oxidative stress with increased production of reactive oxygen species (ROS) has been implicated in a wide variety of pathological conditions, including inflammation and many cardiovascular diseases. It is thus important to identify the role of ROS and their mechanistic significance in microvessel barrier dysfunction under pathological conditions. The role of specific ROS and their cross talk in pathological processes is complex. The mechanisms of ROS-induced increases in vascular permeability remain poorly understood. The sources of ROS in diseases have been extensively reviewed at enzyme levels. This review will instead focus on the underlying mechanisms of ROS release by leukocytes, the differentiate effects and signaling mechanisms of individual ROS on endothelial cells, pericytes and microvessel barrier function, as well as the interplay of reactive oxygen species, nitric oxide, and nitrogen species in ROS-mediated vascular barrier dysfunction. As a counter balance of excessive ROS, nuclear factor erythroid 2 related factor 2 (Nrf2), a redox-sensitive cell-protective transcription factor, will be highlighted as a potential therapeutic target for antioxidant defenses. The advantages and limitations of different experimental approaches used for the study of ROS-induced endothelial barrier function are also discussed. This article will outline the advances emerged mainly from

Indexed as

microvessel permeabilityNrf-2pericytereactive nitrogen speciesreactive oxygen species

Identifiers

PMID32536875
PMCPMC7268512
OpenAlexW3032317923

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.