Evidence map›Paper›PMID 27564666›Full record

ReviewAnnals of the American Thoracic Society2016

Alpha-1 Antitrypsin Investigations Using Animal Models of Emphysema.

Kevin Ni, Karina A Serban, Chanan Batra, Irina Petrache

Open access · greenAbstract readReview
In one paragraph

Review 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 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

8 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Role for Cela1 in Postnatal Lung Remodeling and Alpha-1 Antitrypsin-Deficient Emphysema.American journal of respiratory cell and molecular biology · 2018
    Article
  8. Mouse Models of COPD.Methods in molecular biology (Clifton, N.J.) · 2018
    Article
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

4 authors at 1 institution in 1 country.

Kevin NiDepartment of Medicine, Division of Pulmonary, Critical Care, and Sleep Medicine, National Jewish Health, Denver, Colorado.ORCID 0000-0002-9707-3091
Karina A SerbanDepartment of Medicine, Division of Pulmonary, Critical Care, and Sleep Medicine, National Jewish Health, Denver, Colorado.ORCID 0000-0002-9372-3034
Chanan BatraDepartment of Medicine, Division of Pulmonary, Critical Care, and Sleep Medicine, National Jewish Health, Denver, Colorado.
Irina PetracheDepartment of Medicine, Division of Pulmonary, Critical Care, and Sleep Medicine, National Jewish Health, Denver, Colorado.ORCID 0000-0003-1094-2600
National Jewish Health · US

Funding

Ceramide-induced Lung Destruction in EmphysemaR01HL077328 · NHLBI · NATIONAL JEWISH HEALTH · PI PETRACHE, IRINA · 2006 to 2024
$8.0M
IU Training Program in Molecular Physiology and Clinical Mechanisms of Lung DiseaseT32HL091816 · NHLBI · INDIANA UNIVERSITY INDIANAPOLIS · PI Erick Forno, Roberto F. Machado · 2009 to 2026
$4.3M
Direct and Bone-Marrow Mediated Effects of Adipose Stem Cells in EmphysemaR01HL105772 · NHLBI · NATIONAL JEWISH HEALTH · PI MARCH, KEITH LEONARD, PETRACHE, IRINA · 2012 to 2015
$1.5M
Optimizing vascular protective effects of antitrypsin in COPDI01BX001150 · VA · RLR VA MEDICAL CENTER · PI PETRACHE, IRINA · 2012 to 2015
–
BLRD VA I01 BX001150NHLBI NIH HHS R01 HL077328NHLBI NIH HHS R01 HL105772NHLBI NIH HHS T32 HL091816
6 · The paper itself

Abstract

Animal models of disease help accelerate the translation of basic science discoveries to the bedside, because they permit experimental interrogation of mechanisms at relatively high throughput, while accounting for the complexity of an intact organism. From the groundbreaking observation of emphysema-like alveolar destruction after direct instillation of elastase in the lungs to the more clinically relevant model of airspace enlargement induced by chronic exposure to cigarette smoke, animal models have advanced our understanding of alpha-1 antitrypsin (AAT) function. Experimental in vivo models that, at least in part, replicate clinical human phenotypes facilitate the translation of mechanistic findings into individuals with chronic obstructive pulmonary disease and with AAT deficiency. In addition, unexpected findings of alveolar enlargement in various transgenic mice have led to novel hypotheses of emphysema development. Previous challenges in manipulating the AAT genes in mice can now be overcome with new transgenic approaches that will likely advance our understanding of functions of this essential, lung-protective serine protease inhibitor (serpin).

Indexed as

Disease Models, Animalalpha 1-Antitrypsinalpha 1-Antitrypsin DeficiencyAnimalsMiceMice, TransgenicPulmonary Disease, Chronic ObstructivePulmonary Emphysemaalpha 1-Antitrypsinalpha-1 antiproteinasechronic obstructive pulmonary diseaseemphysema

Identifiers

PMID27564666
PMCPMC5059494
OpenAlexW2515389810

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.