Evidence map›Paper›PMID 32973162›Full record

ArticleCell death & disease2020

Multi-omics analysis identifies FoxO1 as a regulator of macrophage function through metabolic reprogramming.

Kai Yan, Tian-Tian Da, Zhen-Hua Bian, Yi He, Meng-Chu Liu, Qing-Zhi Liu, Jie Long, Liang Li, Cai-Yue Gao, Shu-Han Yang and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

36 citing papers in PubMed, 47 citations in OpenAlex.

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  13. Acta biochimica et biophysica Sinica · 2024
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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

12 authors at 3 institutions in 1 country.

Kai YanLiver Immunology Laboratory, School of Life Sciences, University of Science and Technology of China, Hefei, 230022, Anhui, China.
Tian-Tian DaChronic Disease Laboratory, Institutes for Life Sciences and School of Medicine, South China University of Technology, Guangzhou, 510006, Guangzhou, China.
Zhen-Hua BianChronic Disease Laboratory, Institutes for Life Sciences and School of Medicine, South China University of Technology, Guangzhou, 510006, Guangzhou, China.
Yi HeDepartment of Rheumatology and Immunology, The Third Affiliated Hospital of Southern Medical University, Guangzhou, 510630, Guangdong, China.
Meng-Chu LiuChronic Disease Laboratory, Institutes for Life Sciences and School of Medicine, South China University of Technology, Guangzhou, 510006, Guangzhou, China.
Qing-Zhi LiuChronic Disease Laboratory, Institutes for Life Sciences and School of Medicine, South China University of Technology, Guangzhou, 510006, Guangzhou, China.
Jie LongLiver Immunology Laboratory, School of Life Sciences, University of Science and Technology of China, Hefei, 230022, Anhui, China.
Liang LiChronic Disease Laboratory, Institutes for Life Sciences and School of Medicine, South China University of Technology, Guangzhou, 510006, Guangzhou, China.
Cai-Yue GaoChronic Disease Laboratory, Institutes for Life Sciences and School of Medicine, South China University of Technology, Guangzhou, 510006, Guangzhou, China.
Shu-Han YangChronic Disease Laboratory, Institutes for Life Sciences and School of Medicine, South China University of Technology, Guangzhou, 510006, Guangzhou, China.
Zhi-Bin ZhaoChronic Disease Laboratory, Institutes for Life Sciences and School of Medicine, South China University of Technology, Guangzhou, 510006, Guangzhou, China. zhaozb@scut.edu.cn.
Zhe-Xiong LianChronic Disease Laboratory, Institutes for Life Sciences and School of Medicine, South China University of Technology, Guangzhou, 510006, Guangzhou, China. zxlian@scut.edu.cn.
South China University of Technology · CNThird Affiliated Hospital of Southern Medical University · CNUniversity of Science and Technology of China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macrophages are plastic cells that can switch among different states according to bioenergetic or biosynthetic requirements. Our previous work demonstrated that the transcription factor Forkhead Box Protein 1 (FoxO1) plays a pivotal role in regulating the function of macrophages, but the underlying mechanisms are still unclear. Here we identify FoxO1 as a regulator of macrophage function through metabolic reprogramming. Transcriptomic and proteomic analyses showed that the deficiency of FoxO1 results in an alternatively activated (M2) phenotype of macrophages, with lower expression of inflammatory response- and migration-associated genes. Using the high content screening and analysis technology, we found that deletion of FoxO1 in macrophages slows their migration rate and impairs their function to limit tumor cell growth in vitro. Next, we demonstrated that glycolysis is inhibited in FoxO1-deficient macrophages, which leads to the observed functional changes and the reduced tumor suppression capability. This prospective study shows that FoxO1 serves as a bridge between metabolism and macrophage function.

Indexed as

Cell BiologyCellular ReprogrammingForkhead Box Protein O1HumansMacrophagesProteomicsForkhead Box Protein O1FOXO1 protein, human

Identifiers

PMID32973162
PMCPMC7518254
OpenAlexW3088927073

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.