Evidence map›Paper›PMID 21029294›Full record

ReviewDiabetes, obesity & metabolism2010

Autophagic pathways and metabolic stress.

S Kaushik, R Singh, A M Cuervo

Open access · bronzeAbstract readReview
In one paragraph

Review in Diabetes, obesity & metabolism, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
4.4field-weighted citation impact, top 5% 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

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 93 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Blockage of Autophagy for Cancer Therapy: A Comprehensive Review.International journal of molecular sciences · 2024
    Review
  4. Review
  5. Article
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  9. Article
  10. Review
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  14. Review
  15. Article
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  17. Iron deficiency as energetic insult to skeletal muscle in chronic diseases.Journal of cachexia, sarcopenia and muscle · 2018
    Review
  18. Article
  19. Article
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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.

S KaushikDepartment of Developmental and Molecular Biology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
R Singh
A M Cuervo
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 MACIAN, FERNANDO · 2009 to 2024
$36.2M
TRANSLATIONAL APPROACHES TO NEUROPROTECTION OF AXONS IN PDrP50NS038370 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI BURKE, ROBERT E · 1999 to 2014
$24.0M
Project4: INTERACTION OF AUTOPHAGIC AND HETEROPHAGIC PATHWAYS IN LIVERP01DK041918 · NIDDK · YESHIVA UNIVERSITY · PI WOLKOFF, ALLAN W · 1990 to 2012
$19.1M
Training in Aging ResearchT32AG023475 · NIA · ALBERT EINSTEIN COL OF MED YESHIVA UNIV · PI NIR J BARZILAI, DEREK Major HUFFMAN · 2004 to 2026
$8.6M
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
Regulation of lipid metabolism by macroautophagyK01DK087776 · NIDDK · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI SINGH, RAJAT · 2010 to 2014
$605k
NIA NIH HHS AG021904NIA NIH HHS AG031782NIA NIH HHS P01 AG031782NIA NIH HHS R01 AG021904NIA NIH HHS R37 AG021904NIA NIH HHS T32 AG023475NIA NIH HHS T32AG023475NIDDK NIH HHS DK041918NIDDK NIH HHS DK087776-01NIDDK NIH HHS K01 DK087776NIDDK NIH HHS P01 DK041918NINDS NIH HHS NS038370NINDS NIH HHS P50 NS038370
6 · The paper itself

Abstract

Autophagy is an essential intracellular process that mediates degradation of intracellular proteins and organelles in lysosomes. Autophagy was initially identified for its role as alternative source of energy when nutrients are scarce but, in recent years, a previously unknown role for this degradative pathway in the cellular response to stress has gained considerable attention. In this review, we focus on the novel findings linking autophagic function with metabolic stress resulting either from proteins or lipids. Proper autophagic activity is required in the cellular defense against proteotoxicity arising in the cytosol and also in the endoplasmic reticulum, where a vast amount of proteins are synthesized and folded. In addition, autophagy contributes to mobilization of intracellular lipid stores and may be central to lipid metabolism in certain cellular conditions. In this review, we focus on the interrelation between autophagy and different types of metabolic stress, specifically the stress resulting from the presence of misbehaving proteins within the cytosol or in the endoplasmic reticulum and the stress following a lipogenic challenge. We also comment on the consequences that chronic exposure to these metabolic stressors could have on autophagic function and on how this effect may underlie the basis of some common metabolic disorders.

Indexed as

AutophagyEndoplasmic ReticulumHumansLipid MetabolismLysosomesProteinsStress, PhysiologicalProteins

Identifiers

PMID21029294
PMCPMC3994321
OpenAlexW2077269293

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.