Evidence map›Paper›PMID 30157433›Full record

ArticleCell reports2018

Mitochondrial Complex I Activity Is Required for Maximal Autophagy.

Hala Elnakat Thomas, Yu Zhang, Jonathan A Stefely, Sonia R Veiga, George Thomas, Sara C Kozma, Carol A Mercer

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
7.6field-weighted citation impact, top 2% 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

62 citing papers in PubMed, 121 citations in OpenAlex.

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  16. Does Autophagy have a Role in the Pathogenesis of Pediatric Hepatic Steatosis?Asian Pacific journal of cancer prevention : APJCP · 2024
    Article
  17. Article
  18. Contrasting views on the role of AMPK in autophagy.BioEssays : news and reviews in molecular, cellular and developmental biology · 2024
    Article
  19. Review
  20. Article

2 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

7 authors at 3 institutions in 2 countries.

Hala Elnakat ThomasDivision of Hematology/Oncology, University of Cincinnati, Cincinnati, OH, USA.
Yu ZhangDivision of Hematology/Oncology, University of Cincinnati, Cincinnati, OH, USA.
Jonathan A StefelyDivision of Hematology/Oncology, University of Cincinnati, Cincinnati, OH, USA; Medical Scientist Training Program, School of Medicine and Public Health, University of Wisconsin-Madison, Madison, WI, USA.
Sonia R VeigaLaboratory of Metabolism and Cancer, Catalan Institute of Oncology, ICO, Bellvitge Biomedical Research Institute, IDIBELL, 08908 Barcelona, Spain.
George ThomasDivision of Hematology/Oncology, University of Cincinnati, Cincinnati, OH, USA; Laboratory of Metabolism and Cancer, Catalan Institute of Oncology, ICO, Bellvitge Biomedical Research Institute, IDIBELL, 08908 Barcelona, Spain; Unit de Biochemistry, Department of Physiological Sciences II, Faculty of Medicine, Campus Universitari de Bellvitge-IDIBELL, University of Barcelona, 08908 L'Hospitalet de Llobregat, Barcelona, Catalonia, Spain.
Sara C KozmaDivision of Hematology/Oncology, University of Cincinnati, Cincinnati, OH, USA; Laboratory of Metabolism and Cancer, Catalan Institute of Oncology, ICO, Bellvitge Biomedical Research Institute, IDIBELL, 08908 Barcelona, Spain.
Carol A MercerDivision of Hematology/Oncology, University of Cincinnati, Cincinnati, OH, USA. Electronic address: mercerc@ucmail.uc.edu.
University of Cincinnati · USInstitut Català d'Oncologia · ESInstitut d'Investigació Biomédica de Bellvitge · ES

Funding

INTEGRATED TRAINING FOR PHYSICIAN-SCIENTISTST32GM008692 · NIGMS · UNIVERSITY OF WISCONSIN-MADISON · PI BURKARD, MARK E · 1998 to 2020
$10.3M
Autophagy, mTOR inhibitors and phenformin in hepatocellular carcinomaR21CA191814 · NCI · UNIVERSITY OF CINCINNATI · PI MERCER, CAROL · 2015 to 2016
$406k
NCI NIH HHS R21 CA191814NIGMS NIH HHS T32 GM008692
6 · The paper itself

Abstract

Cells adapt to nutrient and energy deprivation by inducing autophagy, which is regulated by the mammalian target of rapamycin (mTOR) and AMP-activated protein kinases (AMPKs). We found that cell metabolism significantly influences the ability to induce autophagy, with mitochondrial complex I function being an important factor in the initiation, amplitude, and duration of the response. We show that phenformin or genetic defects in complex I suppressed autophagy induced by mTOR inhibitors, whereas autophagy was enhanced by strategies that increased mitochondrial metabolism. We report that mTOR inhibitors significantly increased select phospholipids and mitochondrial-associated membranes (MAMs) in a complex I-dependent manner. We attribute the complex I autophagy defect to the inability to increase MAMs, limiting phosphatidylserine decarboxylase (PISD) activity and mitochondrial phosphatidylethanolamine (mtPE), which support autophagy. Our data reveal the dynamic and metabolic regulation of autophagy.

Indexed as

AnimalsAutophagyHumansHypoglycemic AgentsMitochondriaPhenforminHypoglycemic AgentsPhenforminAMPKautophagymetabolismmitochondria associated membranemitophagymTORphenforminphosphatidylethanolaminephosphatidylserine decarboxylasephospholipids

Identifiers

PMID30157433
PMCPMC6298213
OpenAlexW2888909823

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.