Evidence map›Paper›PMID 32764389›Full record

ReviewGenes2020

Pathological Consequences of Hepatic mTORC1 Dysregulation.

Chun-Seok Cho, Allison Ho Kowalsky, Jun Hee Lee

Open access · goldAbstract readReview
In one paragraph

Review in Genes, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

11 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Vitamin E andDose-response : a publication of International Hormesis Society
    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.

Chun-Seok ChoDepartment of Molecular & Integrative Physiology, University of Michigan, Ann Arbor, MI 48109, USA.ORCID 0000-0002-9589-5745
Allison Ho KowalskyDepartment of Molecular & Integrative Physiology, University of Michigan, Ann Arbor, MI 48109, USA.ORCID 0000-0002-0922-0910
Jun Hee LeeDepartment of Molecular & Integrative Physiology, University of Michigan, Ann Arbor, MI 48109, USA.ORCID 0000-0002-2200-6011
University of Michigan · US

Funding

Pilot and Feasibility (P and F) ProgramP30DK089503 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI RANDY J SEELEY · 2010 to 2026
$20.3M
Research Training in BiogerontologyT32AG000114 · NIA · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SCOTT PLETCHER · 1985 to 2026
$12.4M
SYTEMS AND INTEGRATIVE BIOLOGYT32GM008322 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LOW, MALCOLM JAMES · 1990 to 2020
$5.7M
Multidisciplinary Training Program in Basic Diabetes ResearchT32DK101357 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PETER ARVAN, Ormond A MacDougald · 2014 to 2026
$4.1M
The molecular mechanisms of nutrient- and stress-dependent mTORC1 regulation mediated by human Sestrin2.R01DK111465 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CHO, UHN-SOO · 2016 to 2020
$2.4M
Mechanisms underlying Hepatoprotective Roles of Sestrin2R01DK102850 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LEE, JUN HEE · 2015 to 2019
$1.7M
Protein inclusions in non-alcoholic steatohepatitisR01DK114131 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LEE, JUN HEE · 2018 to 2020
$1.0M
Defining the Sestrin2-AKT signaling pathway, a novel mechanism in the insulin signaling networkF31DK117610 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KOWALSKY, ALLISON HO · 2018 to 2019
$73k
NIA NIH HHS T32 AG000114NIDDK NIH HHS F31 DK117610NIDDK NIH HHS P30 DK089503NIDDK NIH HHS R01 DK102850NIDDK NIH HHS R01 DK114131NIDDK NIH HHS T32 DK101357NIGMS NIH HHS T32 GM008322
6 · The paper itself

Abstract

The mammalian target of rapamycin complex 1 (mTORC1) is a central regulator of metabolism that integrates environmental inputs, including nutrients, growth factors, and stress signals. mTORC1 activation upregulates anabolism of diverse macromolecules, such as proteins, lipids, and nucleic acids, while downregulating autolysosomal catabolism. mTORC1 dysregulation is often found in various diseases, including cancer, cardiovascular and neurodegenerative diseases, as well as metabolic syndromes involving obesity and type II diabetes. As an essential metabolic organ, the liver requires proper regulation of mTORC1 for maintaining homeostasis and preventing pathologies. For instance, aberrant hyper- or hypoactivation of mTORC1 disrupts hepatocellular homeostasis and damages the structural and functional integrity of the tissue, leading to prominent liver injury and the development of hepatocellular carcinogenesis. Proper regulation of mTORC1 during liver diseases may be beneficial for restoring liver function and ameliorating the detrimental consequences of liver failure.

Indexed as

HomeostasisAnimalsHumansLiverMechanistic Target of Rapamycin Complex 1Signal TransductionMechanistic Target of Rapamycin Complex 1livermetabolismmTORC1

Identifiers

PMID32764389
PMCPMC7465966
OpenAlexW3047111872

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.