Evidence map›Paper›PMID 38017373›Full record

ArticleMolecular medicine (Cambridge, Mass.)2023

IGF2 deficiency promotes liver aging through mitochondrial dysfunction and upregulated CEBPB signaling in D-galactose-induced aging mice.

Xiaohai Zhou, Bowen Tan, Weiwei Gui, Caiping Zhou, Hanxin Zhao, Xihua Lin, Hong Li

Open access · goldAbstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2023. 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
2.6field-weighted citation impact, top 9% 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, 15 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. [Astragaloside IV alleviates D-GAL-induced endothelial cell senescence by promoting mitochondrial autophagyNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025
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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

7 authors at 1 institution in 1 country.

Xiaohai ZhouDepartment of Endocrinology, the Affiliated Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
Bowen TanDepartment of Endocrinology, the Affiliated Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
Weiwei GuiDepartment of Endocrinology, the Affiliated Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
Caiping ZhouDepartment of Endocrinology, the Affiliated Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
Hanxin ZhaoDepartment of Endocrinology, the Affiliated Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
Xihua LinDepartment of Endocrinology, the Affiliated Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, China. linxihua@zju.edu.cn.
Hong LiDepartment of Endocrinology, the Affiliated Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, China. srrshnfm@zju.edu.cn.ORCID 0000-0003-4158-1860
Sir Run Run Shaw Hospital · CN

Funding

Innovative Research Group Project of the National Natural Science Foundation of China 82200638Medical Science and Technology Project of Zhejiang Province 2021RC081
6 · The paper itself

Abstract

backgroundLiver aging, marked by cellular senescence and low-grade inflammation, heightens susceptibility to chronic liver disease and worsens its prognosis. Insulin-like growth factor 2 (IGF2) has been implicated in numerous aging-related diseases. Nevertheless, its role and underlying molecular mechanisms in liver aging remain largely unexplored.

methodsThe expression of IGF2 was examined in the liver of young (2-4 months), middle-aged (9-12 months), and old (24-26 months) C57BL/6 mice. In vivo, we used transgenic IGF2

resultsWe observed a significant reduction of IGF2 levels in the livers of aged mice. Subsequently, we demonstrated that IGF2 deficiency promoted senescence phenotypes and senescence-associated secretory phenotypes (SASPs), both in vitro and in vivo aging models. Moreover, IGF2 deficiency impaired mitochondrial function, reducing mitochondrial respiratory capacity, mitochondrial membrane potential, and nicotinamide adenine dinucleotide (NAD)

conclusionsIn summary, our findings strongly suggest that IGF2 deficiency promotes liver aging through mitochondrial dysfunction and upregulated CEBPB signaling. These results provide compelling evidence for considering IGF2 as a potential target for interventions aimed at slowing down the process of liver aging.

Indexed as

AgingGalactoseAnimalsInsulin-Like Growth Factor IILiverMiceMice, Inbred C57BLMitochondriaGalactoseIGF2 protein, mouseInsulin-Like Growth Factor IIAgingCEBPBIGF2LiverMitochondria dysfunction

Identifiers

PMID38017373
PMCPMC10685569
OpenAlexW4389082608

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.