Evidence map›Paper›PMID 27115949›Full record

ArticleAnnals of the American Thoracic Society2016

Alpha-1 Antitrypsin and Lung Cell Apoptosis.

Karina A Serban, Irina Petrache

Open access · greenAbstract read
In one paragraph

Article in Annals of the American Thoracic Society, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

25 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Alpha-1 antitrypsin inhibits fractalkine-mediated monocyte-lung endothelial cell interactions.American journal of physiology. Lung cellular and molecular physiology · 2023
    Article
  9. Review
  10. Salivary Biomarkers to Differentiate betweenDiagnostics (Basel, Switzerland) · 2023
    Article
  11. Article
  12. Article
  13. Proteolysis and Deficiency of α1-Proteinase Inhibitor in SARS-CoV-2 Infection.Biochemistry (Moscow) Supplement. Series B, Biomedical chemistry · 2022
    Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Dysregulation of the glutaredoxin/American journal of physiology. Cell physiology · 2020
    Article
  19. Lectin Complement Pathway in Emphysema.American journal of respiratory and critical care medicine · 2019
    Article
  20. 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

2 authors at 2 institutions in 1 country.

Karina A SerbanDivision of Pulmonary, Critical Care, and Sleep Medicine, Department of Medicine, National Jewish Health, Denver, Colorado.ORCID 0000-0002-9372-3034
Irina PetracheDivision of Pulmonary, Critical Care, and Sleep Medicine, Department of Medicine, National Jewish Health, Denver, Colorado.
National Jewish Health · USUniversity of Colorado Denver · US

Funding

Optimizing vascular protective effects of antitrypsin in COPDI01BX001150 · VA · RLR VA MEDICAL CENTER · PI PETRACHE, IRINA · 2012 to 2015
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BLRD VA I01 BX001150
6 · The paper itself

Abstract

Discovery of alpha-1 antitrypsin (A1AT) as the principal circulating inhibitor of neutrophil elastase was critical to the appreciation of protease/antiprotease imbalance involvement in the pathogenesis of emphysema. Additional targets of A1AT have been uncovered, along with their contribution to alveolar wall destruction induced by cigarette smoke exposure. We highlight in this report mechanisms of A1AT antiapoptotic effects on structural lung endothelial cells. This function was largely dependent on uptake of the protein from the circulation via clathrin- and, in part, caveolae-mediated endocytosis and on specific interactions with cysteine proteases such as capsase-3, -6, and -7. Exposures to cigarette smoke diminished A1AT intracellular uptake and its anticaspase action, suggesting that even in A1AT-suficient individuals, cigarette smoke may weaken the serpin's endothelial prosurvival effect. In addition, cigarette smoke exposure or genetic mutations known to induce posttranslational modifications such as oxidation or polymerization may alter A1AT bidirectional intracellular traffic in endothelial cells and thus determine its functional bioavailability in certain lung compartments. Uncovering and harnessing the A1AT canonical and noncanonical mechanisms will advance our understanding of the pathogenesis of emphysema and may provide means to improve the effectiveness of therapies in both A1AT-sufficient and A1AT-deficient individuals.

Indexed as

ApoptosisEndocytosisalpha 1-Antitrypsinalpha 1-Antitrypsin DeficiencyAlveolar Epithelial CellsCaspase 3Caspase 6Caspase 7HumansLungPulmonary EmphysemaSmokeTobacco Productsalpha 1-AntitrypsinCASP3 protein, humanCASP6 protein, humanCASP7 protein, humanCaspase 3Caspase 6Caspase 7Smokealpha-1 antitrypsinapoptosiscaspasecigarette smokeemphysema

Identifiers

PMID27115949
PMCPMC5466181
OpenAlexW2342943184

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.