Evidence map›Paper›PMID 26905827›Full record

ReviewCell calcium2016

ROS-activated calcium signaling mechanisms regulating endothelial barrier function.

Anke Di, Dolly Mehta, Asrar B Malik

Abstract readReview
In one paragraph

Review in Cell calcium, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

51 citing papers in PubMed, 80 citations in OpenAlex.

  1. Article
  2. Role of neutrophils in regulating vascular permeability in inflammatory and autoimmune diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
  3. Review
  4. Article
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  6. Article
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  9. Review
  10. Against the Waves: Blocking the EB3-IP3 Interaction Inhibits Calcium Waves in the Lung Endothelium.American journal of respiratory cell and molecular biology · 2023
    Article
  11. Mitochondria of lung venular capillaries mediate lung-liver cross talk in pneumonia.American journal of physiology. Lung cellular and molecular physiology · 2023
    Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Potential Benefits of Nutraceuticals for Oxidative Stress Management.Revista brasileira de farmacognosia : orgao oficial da Sociedade Brasileira de Farmacognosia · 2022
    Review
  18. Anshen Buxin Liuwei Pill, a Mongolian Medicinal Formula, Could Protect HEvidence-based complementary and alternative medicine : eCAM · 2022
    Article
  19. Reactive Oxygen Species and Endothelial CaInternational journal of molecular sciences · 2021
    Review
  20. Endothelial metabolism in pulmonary vascular homeostasis and acute respiratory distress syndrome.American journal of physiology. Lung cellular and molecular physiology · 2021
    Review
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 2 institutions in 1 country.

Anke DiDepartment of Pharmacology, The University of Illinois College of Medicine, Chicago, IL 60612, United States.
Dolly MehtaDepartment of Pharmacology, The University of Illinois College of Medicine, Chicago, IL 60612, United States.
Asrar B MalikDepartment of Pharmacology, The University of Illinois College of Medicine, Chicago, IL 60612, United States. Electronic address: abmalik@uic.edu.
Illinois College · USUniversity of Illinois Urbana-Champaign · US

Funding

TRPC6 Regulation of Lung Endothelial Barrier FunctionP01HL060678 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI MALIK, ASRAR B. · 2000 to 2020
$40.1M
Trpm2 Regulation of Phagocyte Bactericidal Activity and Resolution of Lung InjuryP01HL077806 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI ZHAO, YOU-YANG · 2005 to 2019
$27.0M
Focal Adhesion Kinase Regulation of Lung Vascular Permeability and EdemagenesisR01HL084153 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI MEHTA, DOLLY · 2007 to 2022
$5.4M
Repair mechanisms of sepsis induced endothelial dysfunction and lung injuryR01HL125350 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI MALIK, ASRAR B., ZHAO, YOU-YANG · 2014 to 2018
$3.2M
NHLBI NIH HHS P01 HL060678NHLBI NIH HHS P01 HL077806NHLBI NIH HHS R01 HL084153NHLBI NIH HHS R01 HL125350
6 · The paper itself

Abstract

Increased vascular permeability is a common pathogenic feature in many inflammatory diseases. For example in acute lung injury (ALI) and its most severe form, the acute respiratory distress syndrome (ARDS), lung microvessel endothelia lose their junctional integrity resulting in leakiness of the endothelial barrier and accumulation of protein rich edema. Increased reactive oxygen species (ROS) generated by neutrophils (PMNs) and other inflammatory cells play an important role in increasing endothelial permeability. In essence, multiple inflammatory syndromes are caused by dysfunction and compromise of the barrier properties of the endothelium as a consequence of unregulated acute inflammatory response. This review focuses on the role of ROS signaling in controlling endothelial permeability with particular focus on ALI. We summarize below recent progress in defining signaling events leading to increased endothelial permeability and ALI.

Indexed as

Calcium SignalingAnimalsCapillary PermeabilityCell Membrane PermeabilityEndotheliumHumansModels, BiologicalReactive Oxygen SpeciesReactive Oxygen Species

Identifiers

PMID26905827
PMCPMC4988951
OpenAlexW2282424977

What OpenQuestion holds

Textmetadata
LicenceTDM
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.