Evidence map›Paper›PMID 30717487›Full record

ReviewCells2019

Protective Features of Autophagy in Pulmonary Infection and Inflammatory Diseases.

Kui Wang, Yi Chen, Pengju Zhang, Ping Lin, Na Xie, Min Wu

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2019. 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
7.3field-weighted citation impact, top 2% 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, 79 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Autophagy, cell death, and cytokines inEmerging microbes & infections · 2023
    Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Role of autophagy in lung diseases and ageing.European respiratory review : an official journal of the European Respiratory Society · 2022
    Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. 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

6 authors at 3 institutions in 2 countries.

Kui WangWest China School of Basic Medical Sciences & Forensic Medicine, and State Key Laboratory of Biotherapy, Sichuan University, and Collaborative Innovation Center for Biotherapy, Chengdu 610041, China. wangkui416@163.com.
Yi ChenDepartment of Gastrointestinal Surgery, State Key Laboratory of Biotherapy, Sichuan University, Chengdu, 610041, China. toddychan@163.com.
Pengju ZhangWest China School of Basic Medical Sciences & Forensic Medicine, and State Key Laboratory of Biotherapy, Sichuan University, and Collaborative Innovation Center for Biotherapy, Chengdu 610041, China. zhangpengju526@163.com.
Ping LinDepartment of Biomedical Sciences, University of North Dakota, Grand Forks, ND 58203, USA. bio_lp@126.com.
Na XieWest China School of Basic Medical Sciences & Forensic Medicine, and State Key Laboratory of Biotherapy, Sichuan University, and Collaborative Innovation Center for Biotherapy, Chengdu 610041, China. xnshina@126.com.
Min WuDepartment of Biomedical Sciences, University of North Dakota, Grand Forks, ND 58203, USA. min.wu@med.und.edu.
Sichuan University · CNUniversity of North Dakota · USUniversity of Southern California · US

Funding

Yersina perstis interactions with macrophagesP20GM113123 · NIGMS · UNIVERSITY OF NORTH DAKOTA · PI COMBS, COLIN K · 2016 to 2025
$19.9M
Lung innate immunity against bacterial infectionR01AI109317 · NIAID · UNIVERSITY OF NORTH DAKOTA · PI WU, MIN · 2014 to 2018
$1.7M
Long noncoding RNAs interact with miRNAs to regulate inflammatory responseR01AI138203 · NIAID · UNIVERSITY OF NORTH DAKOTA · PI COMBS, COLIN K · 2018 to 2021
$1.4M
NIAID NIH HHS R01 AI109317NIAID NIH HHS R01 AI138203NIGMS NIH HHS P20 GM113123
6 · The paper itself

Abstract

Autophagy is a highly conserved catabolic process involving autolysosomal degradation of cellular components, including protein aggregates, damaged organelles (such as mitochondria, endoplasmic reticulum, and others), as well as various pathogens. Thus, the autophagy pathway represents a major adaptive response for the maintenance of cellular and tissue homeostasis in response to numerous cellular stressors. A growing body of evidence suggests that autophagy is closely associated with diverse human diseases. Specifically, acute lung injury (ALI) and inflammatory responses caused by bacterial infection or xenobiotic inhalation (e.g., chlorine and cigarette smoke) have been reported to involve a spectrum of alterations in autophagy phenotypes. The role of autophagy in pulmonary infection and inflammatory diseases could be protective or harmful dependent on the conditions. In this review, we describe recent advances regarding the protective features of autophagy in pulmonary diseases, with a focus on ALI, idiopathic pulmonary fibrosis (IPF), chronic obstructive pulmonary disease (COPD), tuberculosis, pulmonary arterial hypertension (PAH) and cystic fibrosis.

Indexed as

AutophagyAnimalsHumansInflammationModels, BiologicalRespiratory Tract InfectionsAutophagy, inflammation, acute lung injury, idiopathic pulmonary fibrosis, COPD, tuberculosis, PAH, cystic fibrosis

Identifiers

PMID30717487
PMCPMC6406971
OpenAlexW2912815602

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.