Evidence map›Paper›PMID 32712601›Full record

ArticleAging2020

Decreased autophagy and fuel switching occur in a senescent hepatic cell model system.

Brijesh Kumar Singh, Madhulika Tripathi, Reddemma Sandireddy, Keziah Tikno, Jin Zhou, Paul Michael Yen

Open access · greenAbstract read
In one paragraph

Article in Aging, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

17 citing papers in PubMed, 28 citations in OpenAlex.

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  11. Selenoproteins and the senescence-associated epitranscriptome.Experimental biology and medicine (Maywood, N.J.) · 2022
    Review
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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

6 authors at 1 institution in 2 countries.

Brijesh Kumar SinghCardiovascular and Metabolic Disorders Program, Duke-NUS Medical School, Singapore 169857, Singapore.
Madhulika TripathiCardiovascular and Metabolic Disorders Program, Duke-NUS Medical School, Singapore 169857, Singapore.
Reddemma SandireddyCardiovascular and Metabolic Disorders Program, Duke-NUS Medical School, Singapore 169857, Singapore.
Keziah TiknoCardiovascular and Metabolic Disorders Program, Duke-NUS Medical School, Singapore 169857, Singapore.
Jin ZhouCardiovascular and Metabolic Disorders Program, Duke-NUS Medical School, Singapore 169857, Singapore.
Paul Michael YenCardiovascular and Metabolic Disorders Program, Duke-NUS Medical School, Singapore 169857, Singapore.
Duke-NUS Medical School · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although aging in the liver contributes to the development of chronic liver diseases such as NAFLD and insulin resistance, little is known about the molecular and metabolic details of aging in hepatic cells. To examine these issues, we used sequential oxidative stress with hydrogen peroxide to induce premature senescence in AML12 hepatic cells. The senescent cells exhibited molecular and metabolic signatures, increased SA-βGal and γH2A.X staining, and elevated senescence and pro-inflammatory gene expression that resembled livers from aged mice. Metabolic phenotyping showed fuel switching towards glycolysis and mitochondrial glutamine oxidation as well as impaired energy production. The senescent AML12 cells also had increased mTOR signaling and decreased autophagy which likely contributed to the fuel switching from β-oxidation that occurred in normal AML12 cells. Additionally, senescence-associated secretory phenotype (SASP) proteins from conditioned media of senescent cells sensitized normal AML12 cells to palmitate-induced toxicity, a known pathological effect of hepatic aging. In summary, we have generated senescent AML12 cells which displayed the molecular hallmarks of aging and also exhibited the aberrant metabolic phenotype, mitochondrial function, and cell signaling that occur in the aged liver.

Indexed as

AgingAnimalsAutophagyCell LineCellular SenescenceEnergy MetabolismGene Expression RegulationGlutamineGlycolysisHepatitisHepatocytesLipid MetabolismLiverMaleMiceMice, Inbred C57BLGlutaminemTOR protein, mouseTOR Serine-Threonine KinasesagingAML12 cellslivermetabolismsenescence

Identifiers

PMID32712601
PMCPMC7425478
OpenAlexW3045066227

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.