Evidence map›Paper›PMID 36139445›Full record

ArticleCells2022

Exosome Release by Glucose Deprivation Is Important for the Viability of TSC-Null Cells.

Ji-Hyun Bae, Jong Hyun Kim

Open access · goldAbstract read
In one paragraph

Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.2field-weighted citation impact, top 46% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Review
  2. Review
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.

Ji-Hyun BaeDepartment of Biochemistry, School of Medicine, Daegu Catholic University, Daegu 42472, Korea.
Jong Hyun KimDepartment of Biochemistry, School of Medicine, Daegu Catholic University, Daegu 42472, Korea.ORCID 0000-0002-0031-5737
Daegu Catholic University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The control of exosome release is associated with numerous physiological and pathological activities, and that release is often indicative of health, disease, and environmental nutrient stress. Tuberous sclerosis complex (TSC) regulates the cell viability via the negative regulation of the mammalian target of rapamycin complex (mTORC1) during glucose deprivation. However, the mechanism by which viability of TSC-null cells is regulated by mTORC1 inhibition under glucose deprivation remains unclear. Here, we demonstrated that exosome release regulates cell death induced by glucose deprivation in TSC-null cells. The mTORC1 inhibition by rapamycin significantly increased the exosome biogenesis, exosome secretion, and cell viability in TSC-null cells. In addition, the increase in cell viability by mTORC1 inhibition was attenuated by two different types of inhibitors of exosome release under glucose deprivation. Taken together, we suggest that exosome release inhibition might be a novel way for regression of cell growth in TSC-null cells showing lack of cell death by mTORC1 inhibition.

Indexed as

ExosomesFibroblastsAnimalsCell SurvivalGlucoseHumansMechanistic Target of Rapamycin Complex 1MiceSirolimusTOR Serine-Threonine KinasesTuberous Sclerosis Complex 1 ProteinTuberous Sclerosis Complex 2 ProteinTumor Suppressor ProteinsGlucoseMechanistic Target of Rapamycin Complex 1SirolimusTOR Serine-Threonine KinasesTuberous Sclerosis Complex 1 ProteinTuberous Sclerosis Complex 2 ProteinTumor Suppressor Proteinscell viabilityexosomeglucose deprivationmTORC1TSC

Identifiers

PMID36139445
PMCPMC9497210
OpenAlexW4295766171

What OpenQuestion holds

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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.