Evidence map›Paper›PMID 36499271›Full record

ArticleInternational journal of molecular sciences2022

Coordination of the AMPK, Akt, mTOR, and p53 Pathways under Glucose Starvation.

Yifan Zhou, Feng Liu

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

12 citing papers in PubMed, 24 citations in OpenAlex.

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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

2 authors at 1 institution in 1 country.

Yifan ZhouNational Laboratory of Solid State Microstructures, Department of Physics, Collaborative Innovation Center of Advanced Microstructures, and Institute for Brain Sciences, Nanjing University, Nanjing 210093, China.
Feng LiuNational Laboratory of Solid State Microstructures, Department of Physics, Collaborative Innovation Center of Advanced Microstructures, and Institute for Brain Sciences, Nanjing University, Nanjing 210093, China.ORCID 0000-0001-9560-8518
Collaborative Innovation Center of Advanced Microstructures · CN

Funding

National Natural Science Foundation of China 11874209
6 · The paper itself

Abstract

Glucose is a direct energy source for eukaryotic cells, and its deficiency elicits complex stress responses and diverse cellular outcomes. Although several signaling pathways involved have been identified, how they coordinately dictate the cell fate remains obscure. We propose a minimal network model for the cellular response to glucose restriction, characterizing the glucose uptake and signaling of the AMPK, Akt, mTOR, and p53 pathways. We demonstrate that in the presence of sufficient growth factors and amino acids, cells may undergo proliferation, senescence, or apoptosis, depending on the extracellular glucose level. AMPK is first activated upon glucose limitation, activating p53 to induce cell-cycle arrest; possibly, cells resume proliferation after timely glucose restoration. For long-term energy stress, cell senescence is maintained by low/intermediate levels of p53 and persistent activation of mTOR and Akt, or cells commit apoptosis when the proteins undergo biphasic dynamics, e.g., p53 switches from intermediate levels to high levels while mTOR and Akt become inactivated in the later phase. The biphasic dynamics of p53 are associated with flipping of two bistable switches. Appropriate mTOR levels are required for optimal cell-fate decision. This work suggests that senescence and apoptosis occur sequentially in glucose-depleted cells, and a theoretical framework is provided for exploring the cellular response to energy stress.

Indexed as

GlucoseTumor Suppressor Protein p53ApoptosisCellular SenescenceProto-Oncogene Proteins c-aktSignal TransductionGlucoseProto-Oncogene Proteins c-aktTumor Suppressor Protein p53apoptosisbiphasic dynamicscell-fate decisionglucose starvationnetwork modelingsenescence

Identifiers

PMID36499271
PMCPMC9741397
OpenAlexW4310995926

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.