Evidence map›Paper›PMID 24192609›Full record

ReviewNature reviews. Gastroenterology & hepatology2014

Liver autophagy: much more than just taking out the trash.

Jaime L Schneider, Ana Maria Cuervo

Abstract readReview
In one paragraph

Review in Nature reviews. Gastroenterology & hepatology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
106citing papers in PubMed, 1 pooled it
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

106 citing papers in PubMed, 1 synthesis or guideline pooled it, 180 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Liver, ageing and disease.Nature reviews. Gastroenterology & hepatology · 2025
    Review
  6. Article
  7. Roles of the Keap1/Nrf2 pathway and mitophagy in liver diseases.Journal of Zhejiang University. Science. B · 2025
    Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. Review
  18. Review
  19. Review
  20. Review

46 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 1 institution in 1 country.

Jaime L SchneiderDepartment of Developmental and Molecular Biology, Institute for Aging Studies, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, New York, NY 10461, USA.
Ana Maria CuervoDepartment of Developmental and Molecular Biology, Institute for Aging Studies, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, New York, NY 10461, USA.
Albert Einstein College of Medicine · US

Funding

Role of Autophagy in T Cell Function and Immunosenescence (Project 3)P01AG031782 · NIA · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI CUERVO, ANA MARIA · 2009 to 2024
$36.2M
MEDICAL SCIENTIST TRAINING PROGRAMT32GM007288 · NIGMS · YESHIVA UNIVERSITY · PI AKABAS, MYLES H. · 1985 to 2022
$35.6M
Control of vesicular trafficking in the hepatocyte.R01DK098408 · NIDDK · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI CUERVO, ANA MARIA, WOLKOFF, ALLAN W · 2013 to 2022
$5.6M
IN VITRO BIOSYNTHESIS OF INSULIN AND GLUCAGONR01DK021860 · NIDDK · YESHIVA UNIVERSITY · PI CUERVO, ANA MARIA · 1986 to 2008
$5.3M
Molecular NeuropathologyT32NS007098 · NINDS · YESHIVA UNIVERSITY · PI SANTAMBROGIO, LAURA · 1985 to 2015
$5.0M
Decreased Protein Degradation in AgingR37AG021904 · NIA · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI CUERVO, ANA MARIA · 2013 to 2022
$4.4M
DECREASED PROTEIN DEGRADATION IN AGINGR01AG021904 · NIA · YESHIVA UNIVERSITY · PI CUERVO, ANA MARIA · 2003 to 2012
$3.7M
The role of chaperone-mediated autophagy in vivoF30AG046109 · NIA · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI SCHNEIDER, JAIME L · 2013 to 2014
$95k
NIA NIH HHS AG031782NIA NIH HHS F30 AG046109NIA NIH HHS F30-AG046109NIA NIH HHS NIH AG21904NIA NIH HHS P01 AG031782NIA NIH HHS R01 AG021904NIA NIH HHS R37 AG021904NIDDK NIH HHS DK098408NIDDK NIH HHS R01 DK021860NIDDK NIH HHS R01 DK098408NIGMS NIH HHS T32 GM007288NIGMS NIH HHS T32-GM007288NINDS NIH HHS NIH/NIA T32-NS007098NINDS NIH HHS T32 NS007098
6 · The paper itself

Abstract

Studies performed in the liver in the 1960s led to the identification of lysosomes and the discovery of autophagy, the process by which intracellular proteins and organelles are degraded in lysosomes. Early studies in hepatocytes also uncovered how nutritional status regulates autophagy and how various circulating hormones modulate the activity of this catabolic process in the liver. The intensive characterization of hepatic autophagy over the years has revealed that lysosome-mediated degradation is important not only for maintaining liver homeostasis in normal physiological conditions, but also for an adequate response of this organ to stressors such as proteotoxicity, metabolic dysregulation, infection and carcinogenesis. Autophagic malfunction has also been implicated in the pathogenesis of common liver diseases, suggesting that chemical manipulation of this process might hold potential therapeutic value. In this Review--intended as an introduction to the topic of hepatic autophagy for clinical scientists--we describe the different types of hepatic autophagy, their role in maintaining homeostasis in a healthy liver and the contribution of autophagic malfunction to liver disease.

Indexed as

AutophagyHepatocytesHumansLiverLiver DiseasesLysosomes

Identifiers

PMID24192609
PMCPMC3980679
OpenAlexW2078881478

What OpenQuestion holds

Textmetadata
LicenceTDM
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.