Evidence map›Paper›PMID 27925481›Full record

ReviewCanadian journal of physiology and pharmacology2017

Mitochondrial ROS, uncoupled from ATP synthesis, determine endothelial activation for both physiological recruitment of patrolling cells and pathological recruitment of inflammatory cells.

Xinyuan Li, Pu Fang, William Y Yang, Kylie Chan, Muriel Lavallee, Keman Xu, Tracy Gao, Hong Wang, Xiaofeng Yang

Abstract readReview
In one paragraph

Review in Canadian journal of physiology and pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
4.4field-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

54 citing papers in PubMed, 78 citations in OpenAlex.

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  17. 29 mJournal of immunology research · 2022
    Article
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  20. Direct cell reprogramming: approaches, mechanisms and progress.Nature reviews. Molecular cell biology · 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

9 authors at 1 institution in 1 country.

Xinyuan LiCenters for Metabolic Disease Research, Cardiovascular Research, and Thrombosis Research, Department of Pharmacology, Lewis Katz School of Medicine at Temple University, Philadelphia, PA 19140, USA.
Pu FangCenters for Metabolic Disease Research, Cardiovascular Research, and Thrombosis Research, Department of Pharmacology, Lewis Katz School of Medicine at Temple University, Philadelphia, PA 19140, USA.
William Y YangCenters for Metabolic Disease Research, Cardiovascular Research, and Thrombosis Research, Department of Pharmacology, Lewis Katz School of Medicine at Temple University, Philadelphia, PA 19140, USA.
Kylie ChanCenters for Metabolic Disease Research, Cardiovascular Research, and Thrombosis Research, Department of Pharmacology, Lewis Katz School of Medicine at Temple University, Philadelphia, PA 19140, USA.
Muriel LavalleeCenters for Metabolic Disease Research, Cardiovascular Research, and Thrombosis Research, Department of Pharmacology, Lewis Katz School of Medicine at Temple University, Philadelphia, PA 19140, USA.
Keman XuCenters for Metabolic Disease Research, Cardiovascular Research, and Thrombosis Research, Department of Pharmacology, Lewis Katz School of Medicine at Temple University, Philadelphia, PA 19140, USA.
Tracy GaoCenters for Metabolic Disease Research, Cardiovascular Research, and Thrombosis Research, Department of Pharmacology, Lewis Katz School of Medicine at Temple University, Philadelphia, PA 19140, USA.
Hong WangCenters for Metabolic Disease Research, Cardiovascular Research, and Thrombosis Research, Department of Pharmacology, Lewis Katz School of Medicine at Temple University, Philadelphia, PA 19140, USA.
Xiaofeng YangCenters for Metabolic Disease Research, Cardiovascular Research, and Thrombosis Research, Department of Pharmacology, Lewis Katz School of Medicine at Temple University, Philadelphia, PA 19140, USA.
Temple University · US

Funding

CD40 monocyte in chronic kidney diseaseR01DK113775 · NIDDK · TEMPLE UNIV OF THE COMMONWEALTH · PI WANG, HONG · 2017 to 2021
$3.3M
Hyperhomocysteinemia and HDL MetabolismR01HL117654 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI WANG, HONG · 2013 to 2017
$3.0M
Caspase-1 activation mediates chronic kidney disease-accelerated atherosclerosisR01HL131460 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI CHOI, ERIC T., WANG, HONG · 2016 to 2019
$2.8M
The roles of miR-155 in regulating atherosclerosis and metabolically healthy obesityR01HL138749 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI YANG, XIAOFENG · 2017 to 2020
$2.6M
Atherogenic roles of complement systemR01HL130233 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI QIN, XUEBIN, WANG, HONG · 2016 to 2019
$2.5M
IL-35 suppression of endothelial cell activation and atherosclerosisR01HL132399 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI YANG, XIAOFENG · 2017 to 2020
$2.3M
HHcy-induced Inflammatory Monocyte and Macrophage Differentiation in DiabetesR01DK104116 · NIDDK · TEMPLE UNIV OF THE COMMONWEALTH · PI WANG, HONG · 2015 to 2019
$2.2M
Roles of Interleukin-17 in Endothelial CellsR01HL108910 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI YANG, XIAOFENG · 2011 to 2015
$1.9M
Suppression of vascular endothelial cell inflammationR01HL094451 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI YANG, XIAOFENG · 2009 to 2013
$1.8M
HHcy-induced Bax upregulation, Treg apoptosis and vascular diseaseR01HL116917 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI YANG, XIAOFENG · 2013 to 2016
$1.6M
NHLBI NIH HHS R01 HL094451NHLBI NIH HHS R01 HL108910NHLBI NIH HHS R01 HL116917NHLBI NIH HHS R01 HL117654NHLBI NIH HHS R01 HL130233NHLBI NIH HHS R01 HL131460NHLBI NIH HHS R01 HL132399NHLBI NIH HHS R01 HL138749NIDDK NIH HHS R01 DK104116NIDDK NIH HHS R01 DK113775
6 · The paper itself

Abstract

Mitochondrial reactive oxygen species (mtROS) are signaling molecules, which drive inflammatory cytokine production and T cell activation. In addition, cardiovascular diseases, cancers, and autoimmune diseases all share a common feature of increased mtROS level. Both mtROS and ATP are produced as a result of electron transport chain activity, but it remains enigmatic whether mtROS could be generated independently from ATP synthesis. A recent study shed light on this important question and found that, during endothelial cell (EC) activation, mtROS could be upregulated in a proton leak-coupled, but ATP synthesis-uncoupled manner. As a result, EC could upregulate mtROS production for physiological EC activation without compromising mitochondrial membrane potential and ATP generation, and consequently without causing mitochondrial damage and EC death. Thus, a novel pathophysiological role of proton leak in driving mtROS production was uncovered for low grade EC activation, patrolling immunosurveillance cell trans-endothelial migration and other signaling events without compromising cellular survival. This new working model explains how mtROS could be increasingly generated independently from ATP synthesis and endothelial damage or death. Mapping the connections among mitochondrial metabolism, physiological EC activation, patrolling cell migration, and pathological inflammation is significant towards the development of novel therapies for inflammatory diseases and cancers.

Indexed as

Energy MetabolismOxidative StressAdenosine TriphosphateAnimalsCardiovascular DiseasesEndothelium, VascularHumansInflammationInflammation MediatorsMembrane Potential, MitochondrialMitochondriaReactive Oxygen SpeciesTransendothelial and Transepithelial MigrationAdenosine TriphosphateInflammation MediatorsReactive Oxygen Speciescancercardiovascular diseasedérivés réactifs de l’oxygèneinflammation vasculairemaladies cardiovasculairesmitochondriamitochondrieROSvascular inflammation

Identifiers

PMID27925481
PMCPMC5336492
OpenAlexW2547798587

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.