Evidence map›Paper›PMID 25617802›Full record

ArticleRedox biology2015

Autophagy in lung disease pathogenesis and therapeutics.

Stefan W Ryter, Augustine M K Choi

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
9.4field-weighted citation impact, top 1% 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

64 citing papers in PubMed, 130 citations in OpenAlex.

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  13. High-altitude hypoxia-induced rat alveolar cell injury by increasing autophagy.International journal of experimental pathology · 2022
    Article
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4 more citing papers are in PubMed but not listed here.

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.

Stefan W RyterJoan and Sanford I. Weill Department of Medicine, Weill Cornell Medical College and New York-Presbyterian Hospital, New York, NY, USA. Electronic address: Str2020@med.cornell.edu.
Augustine M K ChoiJoan and Sanford I. Weill Department of Medicine, Weill Cornell Medical College and New York-Presbyterian Hospital, New York, NY, USA.
Cornell University · USPresbyterian Hospital · US

Funding

Respiratory Computational Discovery CoreP01HL114501 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI CHOI, MARY E · 2013 to 2025
$24.9M
Mesenchymal Stromal Cell Conditioning by Carbon MonoxideP01HL108801 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI CHOI, AUGUSTINE M · 2011 to 2015
$13.8M
HEME OXYGENASE 1--LUNG VASCULAR CELL HYPOXIC RESPONSER01HL060234 · NHLBI · YALE UNIVERSITY · PI CHOI, AUGUSTINE M, CHOI, MARY E · 1999 to 2017
$5.8M
Heme oxygenase-1: Regulation and Function in CaveolaeR01HL079904 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI CHOI, MARY E · 2005 to 2014
$2.9M
NHLBI NIH HHS P01 HL108801NHLBI NIH HHS P01HL108801NHLBI NIH HHS P01 HL114501NHLBI NIH HHS R01 HL060234NHLBI NIH HHS R01HL060234NHLBI NIH HHS R01 HL079904NHLBI NIH HHS R01HL079904
6 · The paper itself

Abstract

Autophagy, a cellular pathway for the degradation of damaged organelles and proteins, has gained increasing importance in human pulmonary diseases, both as a modulator of pathogenesis and as a potential therapeutic target. In this pathway, cytosolic cargos are sequestered into autophagosomes, which are delivered to the lysosomes where they are enzymatically degraded and then recycled as metabolic precursors. Autophagy exerts an important effector function in the regulation of inflammation, and immune system functions. Selective pathways for autophagic degradation of cargoes may have variable significance in disease pathogenesis. Among these, the autophagic clearance of bacteria (xenophagy) may represent a crucial host defense mechanism in the pathogenesis of sepsis and inflammatory diseases. Our recent studies indicate that the autophagic clearance of mitochondria, a potentially protective program, may aggravate the pathogenesis of chronic obstructive pulmonary disease by activating cell death programs. We report similar findings with respect to the autophagic clearance of cilia components, which can contribute to airways dysfunction in chronic lung disease. In certain diseases such as pulmonary hypertension, autophagy may confer protection by modulating proliferation and cell death. In other disorders, such as idiopathic pulmonary fibrosis and cystic fibrosis, impaired autophagy may contribute to pathogenesis. In lung cancer, autophagy has multiple consequences by limiting carcinogenesis, modulating therapeutic effectiveness, and promoting tumor cell survival. In this review we highlight the multiple functions of autophagy and its selective autophagy subtypes that may be of significance to the pathogenesis of human disease, with an emphasis on lung disease and therapeutics.

Indexed as

AutophagyAcute Lung InjuryAnti-Inflammatory AgentsAntioxidantsApoptosis Regulatory ProteinsCystic FibrosisGene Expression RegulationHumansHypertension, PulmonaryIdiopathic Pulmonary FibrosisLung NeoplasmsLysosomesMicrofilament ProteinsPhagosomesPulmonary Disease, Chronic ObstructiveReactive Oxygen SpeciesAnti-Inflammatory AgentsAntioxidantsApoptosis Regulatory ProteinsMicrofilament ProteinsReactive Oxygen SpeciesAutophagyCigarette smokeLung diseaseMitophagyReactive oxygen species

Identifiers

PMID25617802
PMCPMC4803789
OpenAlexW1987988563

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.