Evidence map›Paper›PMID 31652893›Full record

ReviewCells2019

Chaperone-Mediated Autophagy in the Liver: Good or Bad?

Srikanta Dash, Yucel Aydin, Krzysztof Moroz

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 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

27 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Review
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  15. Review
  16. Review
  17. Article
  18. Review
  19. Autophagy in liver diseases.World journal of hepatology · 2021
    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

3 authors at 1 institution in 1 country.

Srikanta DashDepartment of Pathology and Laboratory Medicine, Tulane University Health Sciences Center, 1430 Tulane Avenue, New Orleans, LA 70112, USA. sdash@tulane.edu.
Yucel AydinDepartment of Pathology and Laboratory Medicine, Tulane University Health Sciences Center, 1430 Tulane Avenue, New Orleans, LA 70112, USA. yaydin@tulane.edu.ORCID 0000-0001-6727-6296
Krzysztof MorozDepartment of Pathology and Laboratory Medicine, Tulane University Health Sciences Center, 1430 Tulane Avenue, New Orleans, LA 70112, USA. kmoroz@tulane.edu.
Tulane University · US

Funding

Tracking & Evaluation CoreU54GM104940 · NIGMS · LSU PENNINGTON BIOMEDICAL RESEARCH CTR · PI JUDD E SHELLITO · 2012 to 2026
$69.1M
Translational Genomics Core (TGC)P20GM121288 · NIGMS · LSU HEALTH SCIENCES CENTER · PI Jennifer Erin Cameron · 2017 to 2026
$22.4M
NIGMS NIH HHS P20 GM121288NIGMS NIH HHS U54 GM104940
6 · The paper itself

Abstract

Hepatitis C virus (HCV) infection triggers autophagy processes, which help clear out the dysfunctional viral and cellular components that would otherwise inhibit the virus replication. Increased cellular autophagy may kill the infected cell and terminate the infection without proper regulation. The mechanism of autophagy regulation during liver disease progression in HCV infection is unclear. The autophagy research has gained a lot of attention recently since autophagy impairment is associated with the development of hepatocellular carcinoma (HCC). Macroautophagy, microautophagy, and chaperone-mediated autophagy (CMA) are three autophagy processes involved in the lysosomal degradation and extracellular release of cytosolic cargoes under excessive stress. Autophagy processes compensate for each other during extreme endoplasmic reticulum (ER) stress to promote host and microbe survival as well as HCC development in the highly stressed microenvironment of the cirrhotic liver. This review describes the molecular details of how excessive cellular stress generated during HCV infection activates CMA to improve cell survival. The pathological implications of stress-related CMA activation resulting in the loss of hepatic innate immunity and tumor suppressors, which are most often observed among cirrhotic patients with HCC, are discussed. The oncogenic cell programming through autophagy regulation initiated by a cytoplasmic virus may facilitate our understanding of HCC mechanisms related to non-viral etiologies and metabolic conditions such as uncontrolled type II diabetes. We propose that a better understanding of how excessive cellular stress leads to cancer through autophagy modulation may allow therapeutic development and early detection of HCC.

Indexed as

AutophagyCarcinoma, HepatocellularCell SurvivalChaperone-Mediated AutophagyDiabetes Mellitus, Type 2Endoplasmic Reticulum StressHepacivirusHepatitis CHepatitis C, ChronicHepatocytesHumansInterferon-alphaLiverLiver NeoplasmsLysosomesNF-E2-Related Factor 2Interferon-alphaNFE2L2 protein, humanNF-E2-Related Factor 2Receptor, Interferon alpha-betachaperone-mediated autophagy (CMA)endoplasmic reticulum stress (ER stress)hepatitis C virus (HCV)hepatocellular carcinoma (HCC)interferon alpha receptor 1 (IFNAR1)nuclear factor erythroid 2-related factor 2 (NRF2)

Identifiers

PMID31652893
PMCPMC6912708
OpenAlexW2982037239

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.