Evidence map›Paper›PMID 32847034›Full record

ReviewCells2020

Autophagy Augmentation to Alleviate Immune Response Dysfunction, and Resolve Respiratory and COVID-19 Exacerbations.

Garrett Pehote, Neeraj Vij

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2020. 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
4.5field-weighted citation impact, top 4% 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, 41 citations in OpenAlex.

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  20. The networks of mAging · 2021
    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

2 authors at 2 institutions in 1 country.

Garrett PehoteMichigan State University College of Osteopathic Medicine, East Lansing, MI 48823, USA.ORCID 0000-0003-2327-5747
Neeraj VijDepartment of Pediatrics and Pulmonary Medicine, the Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.ORCID 0000-0002-1976-5340
Johns Hopkins University · USMichigan State University · US

Funding

Mechanisms of VCP/p97 and Proteasomal pathway in COPD pathogenesisR03HL096931 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI VIJ, NEERAJ · 2009 to 2010
$164k
NHLBI NIH HHS R03 HL096931
6 · The paper itself

Abstract

The preservation of cellular homeostasis requires the synthesis of new proteins (proteostasis) and organelles, and the effective removal of misfolded or impaired proteins and cellular debris. This cellular homeostasis involves two key proteostasis mechanisms, the ubiquitin proteasome system and the autophagy-lysosome pathway. These catabolic pathways have been known to be involved in respiratory exacerbations and the pathogenesis of various lung diseases, such as chronic obstructive pulmonary disease (COPD), cystic fibrosis (CF), idiopathic pulmonary fibrosis (IPF), acute lung injury (ALI), acute respiratory distress syndrome (ARDS), and coronavirus disease-2019 (COVID-19). Briefly, proteostasis and autophagy processes are known to decline over time with age, cigarette or biomass smoke exposure, and/or influenced by underlying genetic factors, resulting in the accumulation of misfolded proteins and cellular debris, elevating apoptosis and cellular senescence, and initiating the pathogenesis of acute or chronic lung disease. Moreover, autophagic dysfunction results in an impaired microbial clearance, post-bacterial and/or viral infection(s) which contribute to the initiation of acute and recurrent respiratory exacerbations as well as the progression of chronic obstructive and restrictive lung diseases. In addition, the autophagic dysfunction-mediated cystic fibrosis transmembrane conductance regulator (CFTR) immune response impairment further exacerbates the lung disease. Recent studies demonstrate the therapeutic potential of novel autophagy augmentation strategies, in alleviating the pathogenesis of chronic obstructive or restrictive lung diseases and exacerbations such as those commonly seen in COPD, CF, ALI/ARDS and COVID-19.

Indexed as

BetacoronavirusDisease ProgressionAcute Lung InjuryAutophagyCoronavirus InfectionsCOVID-19Cystic FibrosisCystic Fibrosis Transmembrane Conductance RegulatorHomeostasisHumansIdiopathic Pulmonary FibrosisLysosomesPandemicsPneumonia, ViralPulmonary Disease, Chronic ObstructiveRespiratory Distress SyndromeCFTR protein, humanCystic Fibrosis Transmembrane Conductance RegulatorALIARDSautophagyCFCFTRCOPDCOVID-19exacerbationsIPFSARS-CoV2

Identifiers

PMID32847034
PMCPMC7565665
OpenAlexW3080903629

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.