Evidence map›Paper›PMID 26484418›Full record

ArticleOncotarget2015

4-hydroxynonenal regulates mitochondrial function in human small airway epithelial cells.

Lakshmi Galam, Athena Failla, Ramani Soundararajan, Richard F Lockey, Narasaiah Kolliputi

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.8field-weighted citation impact, top 11% 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

39 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
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  3. Oxeiptosis - potential in cancer treatment?Expert reviews in molecular medicine · 2026
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  5. Article
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  8. Article
  9. Review
  10. Article
  11. [Expression and significance of ferroptosis marker 4-HNE inBeijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2024
    Article
  12. Article
  13. Article
  14. Article
  15. Impact of Lysine Succinylation on the Biology of Fungi.Current issues in molecular biology · 2024
    Review
  16. Review
  17. 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

5 authors at 1 institution in 1 country.

Lakshmi GalamDivision of Allergy and Immunology, Department of Internal Medicine, Morsani College of Medicine, University of South Florida, Tampa, FL, USA.
Athena FaillaDivision of Allergy and Immunology, Department of Internal Medicine, Morsani College of Medicine, University of South Florida, Tampa, FL, USA.
Ramani SoundararajanDivision of Allergy and Immunology, Department of Internal Medicine, Morsani College of Medicine, University of South Florida, Tampa, FL, USA.
Richard F LockeyDivision of Allergy and Immunology, Department of Internal Medicine, Morsani College of Medicine, University of South Florida, Tampa, FL, USA.
Narasaiah KolliputiDivision of Allergy and Immunology, Department of Internal Medicine, Morsani College of Medicine, University of South Florida, Tampa, FL, USA.
University of South Florida · US

Funding

Molecular Mechanisms of Hyperoxic Lung InjuryR01HL105932 · NHLBI · UNIVERSITY OF SOUTH FLORIDA · PI KOLLIPUTI, NARASAIAH · 2011 to 2019
$2.9M
NHLBI NIH HHS R01 HL105932
6 · The paper itself

Abstract

Prolonged exposure to oxidative stress causes Acute Lung Injury (ALI) and significantly impairs pulmonary function. Previously we have demonstrated that mitochondrial dysfunction is a key pathological factor in hyperoxic ALI. While it is known that hyperoxia induces the production of stable, but toxic 4-hydroxynonenal (4-HNE) molecule, it is unknown how the reactive aldehyde disrupts mitochondrial function. Our previous in vivo study indicated that exposure to hyperoxia significantly increases 4-HNE-Protein adducts, as well as levels of MDA in total lung homogenates. Based on the in vivo studies, we explored the effects of 4-HNE in human small airway epithelial cells (SAECs). Human SAECs treated with 25 μM of 4-HNE showed a significant decrease in cellular viability and increased caspase-3 activity. Moreover, 4-HNE treated SAECs showed impaired mitochondrial function and energy production indicated by reduced ATP levels, mitochondrial membrane potential, and aconitase activity. This was followed by a significant decrease in mitochondrial oxygen consumption and depletion of the reserve capacity. The direct effect of 4-HNE on the mitochondrial respiratory chain was confirmed using Rotenone. Furthermore, SAECs treated with 25 μM 4-HNE showed a time-dependent depletion of total Thioredoxin (Trx) proteins and Trx activity. Taken together, our results indicate that 4-HNE induces cellular and mitochondrial dysfunction in human SAECs, leading to an impaired endogenous antioxidant response.

Indexed as

Aconitate HydrataseAdenosine TriphosphateAldehydesAnimalsCaspase 3Cells, CulturedCell SurvivalDose-Response Relationship, DrugEnergy MetabolismEpithelial CellsFemaleHumansHyperoxiaLungMaleMembrane Potential, Mitochondrial4-hydroxy-2-nonenalAconitate HydrataseAdenosine TriphosphateAldehydesCASP3 protein, humanCaspase 3OxidantsThioredoxins4-HNEacute lung injuryhyperoxiaImmune responseImmunityImmunology and Microbiology Sectionmitochondrial dysfunctionROS

Identifiers

PMID26484418
PMCPMC4747170
OpenAlexW1929986647

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.