Evidence map›Paper›PMID 32672471›Full record

ArticleAmerican journal of respiratory cell and molecular biology2020

Mitochondrial Fission Mediated Cigarette Smoke-induced Pulmonary Endothelial Injury.

Zhengke Wang, Alexis White, Xing Wang, Junsuk Ko, Gaurav Choudhary, Thilo Lange, Sharon Rounds, Qing Lu

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

37 citing papers in PubMed, 52 citations in OpenAlex.

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  8. Bioenergetics and metabolism of the pulmonary endothelium. Scientific session I: ReSPIRE 2025.American journal of physiology. Lung cellular and molecular physiology · 2025
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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

8 authors at 3 institutions in 2 countries.

Zhengke WangVascular Research Laboratory, Providence Veterans Affairs Medical Center, Providence, Rhode Island.
Alexis WhiteVascular Research Laboratory, Providence Veterans Affairs Medical Center, Providence, Rhode Island.
Xing WangVascular Research Laboratory, Providence Veterans Affairs Medical Center, Providence, Rhode Island.
Junsuk KoVascular Research Laboratory, Providence Veterans Affairs Medical Center, Providence, Rhode Island.
Gaurav ChoudharyVascular Research Laboratory, Providence Veterans Affairs Medical Center, Providence, Rhode Island.
Thilo LangeVascular Research Laboratory, Providence Veterans Affairs Medical Center, Providence, Rhode Island.
Sharon RoundsVascular Research Laboratory, Providence Veterans Affairs Medical Center, Providence, Rhode Island.
Qing LuVascular Research Laboratory, Providence Veterans Affairs Medical Center, Providence, Rhode Island.
Providence VA Medical Center · USBrown University · USTianjin University · CN

Funding

Uncoupling of IL-1 beta and VEGF-A Crosstalk Contributes to Impaired Arteriogenesis Response to Ischemia in Chronic Diabetes MellitusP20GM103652 · NIGMS · OCEAN STATE RESEARCH INSTITUTE, INC. · PI CHOUDHARY, GAURAV, HARRINGTON, ELIZABETH O · 2013 to 2022
$21.3M
HDAC6 regulates cigarette smoke-induced endothelial barrier dysfunction and lung injuryR01HL130230 · NHLBI · OCEAN STATE RESEARCH INSTITUTE, INC. · PI ROUNDS, SHARON IRENE SMITH · 2016 to 2019
$1.3M
NHLBI NIH HHS R01 HL130230NIGMS NIH HHS P20 GM103652
6 · The paper itself

Abstract

Cigarette smoke (CS) exposure increases the risk for acute respiratory distress syndrome in humans and promotes alveolar-capillary barrier permeability and acute lung injury in animal models. However, the underlying mechanisms are not well understood. Mitochondrial fusion and fission are essential for mitochondrial homeostasis in health and disease. In this study, we hypothesized that CS caused endothelial injury via an imbalance of mitochondrial fusion and fission and resultant mitochondrial oxidative stress and dysfunction. We noted that CS altered mitochondrial morphology by shortening mitochondrial networks and causing perinuclear accumulation of damaged mitochondria in primary rat lung microvascular endothelial cells. We also found that CS increased mitochondrial fission likely by decreasing Drp1-S637 and increasing FIS1, Drp1-S616 phosphorylation, mitochondrial translocation, and tetramerization and reduced mitochondrial fusion likely by decreasing Mfn2 in lung microvascular endothelial cells and mouse lungs. CS also caused aberrant mitophagy, increased mitochondrial oxidative stress, and reduced mitochondrial respiration. An inhibitor of mitochondrial fission and a mitochondria-specific antioxidant prevented CS-induced increased endothelial barrier dysfunction and apoptosis. Our data suggest that excessive mitochondrial fission and resultant oxidative stress are essential mediators of CS-induced endothelial injury and that inhibition of mitochondrial fission and mitochondria-specific antioxidants may be useful therapeutic strategies for CS-induced endothelial injury and associated pulmonary diseases.

Indexed as

Mitochondrial DynamicsAnimalsApoptosisCapillary PermeabilityCell RespirationDynaminsEndothelial CellsLungMaleMiceMicrovesselsMitochondriaMitophagyModels, BiologicalOxidative StressProtein TransportDnm1l protein, mouseDnm1l protein, ratDynaminsapoptosiscigarette smokeendothelial permeabilitymitochondrial fission/fusionmitophagy

Identifiers

PMID32672471
PMCPMC7605166
OpenAlexW3042452150

What OpenQuestion holds

Textmetadata
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.